What Is Acute Inflammation?

In view of the two main components of resistance to pathogenic microorganisms, namely, white blood cells and antibodies, are transported by blood, the three changes in hemodynamics, increased vascular permeability and leukocyte exudation in acute inflammation are very obvious. As a result, protein-rich exudate, fibrin, and leukocytes accumulate in the extravascular space of the injury site. This is the main feature of histopathology of acute inflammation.

Acute inflammation

Acute inflammation

Inflammation can usually be divided into two categories according to the course of the disease: acute inflammation and chronic inflammation. Acute inflammation has a rapid onset and has a short duration, only a few days to a month. It is characterized by exudative lesions, and inflammatory cell infiltration is mainly granulocytes. Chronic inflammation lasts for a long time, constant months to years, and it is often dominated by proliferative lesions. Its inflammatory cell infiltration is dominated by macrophages and lymphocytes.

Chinese name

Acute inflammation

Foreign name

Acute inflammation

Features

Rapid onset and short duration

Histopathological characteristics of acute inflammation

In view of the two main components of resistance to pathogenic microorganisms, namely, white blood cells and antibodies, are transported by blood, the three changes in hemodynamics, increased vascular permeability and leukocyte exudation in acute inflammation are very obvious. As a result, protein-rich exudate, fibrin, and leukocytes accumulate in the extravascular space of the injury site. This is the main feature of histopathology of acute inflammation.

Acute inflammation

Acute inflammatory hemodynamic changes

Hemodynamic changes in the microcirculation after tissue damage occur quickly, that is, changes in the diameter of blood vessels, and the rate of lesion development depends on the severity of the injury. Hemodynamic changes generally occur in the following order.

1. The short arterial contraction injury occurred shortly after the short arterial contraction occurred, lasting only a few seconds. The mechanism may be neurogenic, but certain chemical mediators can also cause vasoconstriction.

2. Vasodilation and accelerated blood flow first involve the arterioles, which subsequently leads to the opening of more microvascular beds and increased local blood flow. This is a sign of hemodynamic changes in the early stages of acute inflammation, and also the cause of local redness and heat.

The mechanism of vasodilation is related to nerve and humoral factors. Neurological factors are called axon reflexes. The humoral factors represented by inflammatory mediators play a more important role in the occurrence of vasodilation.

3 Slowing blood flow is a consequence of increased microvascular permeability. The exudation of protein-rich fluids out of blood vessels results in increased red blood cell concentration and viscosity in blood vessels. The resulting dilated small blood vessels are packed with red blood cells, called stasis.

4 With the appearance of blood cell stagnation, white blood cells in microvascular blood are mainly leukoctytic margination and adhere to endothelial cells. This phenomenon is called leukocyte attachment. Leukocytes then swim out of the blood vessels into the interstitial space by amoebic movement.

Acute inflammation

The time that hemodynamic changes take is related to the type and intensity of the stimulus. The acceleration of blood flow caused by extremely mild stimulation lasts only 10-15 minutes, and then gradually returns to normal; the blood flow is accelerated under mild stimulation for several hours, and then the blood flow becomes slower or even stagnates. Blood flow stagnation occurs in 15 to 30 minutes, and severe injury can often occur in only a few minutes. In addition, the local hemodynamic changes are also related to the distance from the injury factors. For example, the center of the skin burn lesion may have stagnated blood flow, while the peripheral blood vessels are still dilated.

Increased vascular permeability in acute inflammation

In addition to inflammatory edema in the earliest stages of inflammation, which is caused by vasodilatation, increased blood flow speed, increased hydrostatic pressure, and ultrafiltration of plasma, which filters out substantially protein-free liquid from capillaries, it is rich in protein. Exudate production is mainly caused by increased vascular permeability. Due to the large amount of protein reaching the extravascular stroma from the plasma, the colloid osmotic pressure of the plasma decreases, while the tissue colloid osmotic pressure increases, causing a larger amount of fluid to accumulate in the interstitial, thereby forming an inflammatory edema or a serous cavity inflammatory effusion.

The maintenance of microcirculation vascular permeability mainly depends on the integrity of endothelial cells. During inflammation, the following mechanisms can cause increased vascular permeability.

1. Endothelial cell contraction After the binding of histamine, bradykinin, and other inflammatory mediators to endothelial cell receptors, it can rapidly cause endothelial cell contraction, resulting in the formation of a gap between endothelial cells with a width of about 0.5 to 1.0 m. Because these inflammatory mediators have a short half-life of only 15-30 minutes, this response is called an immediate transient response. This reaction affects only the small veins with a diameter of 20 to 60 m, and the small arteries and capillaries are not affected. Antihistamines can suppress this response.

2. Direct endothelium damage, such as severe burns and pyogenic infections, can directly cause endothelial cell damage, causing it to die and fall off. The increase in vascular permeability occurs rapidly and persists at high levels for several hours to several days until thrombus formation in the damaged blood vessels. This process is called an immediate-sustained response. Microcirculation vessels of arterioles, capillaries and venules can be involved.

Mild to moderate thermal damage, X-ray and ultraviolet damage, and direct damage to endothelial cells caused by certain bacterial toxins occur later, often after 2 to 12 hours, but can last for several hours to several days, which is called late Delayed prolonged response. This response affects only capillaries and venules.

3 Leukocyte-mediated endothelial damage In the early stage of inflammation, leukocytes attach to the wall and adhere to endothelial cells, causing leukocyte activation, releasing active oxygen metabolites and proteolytic enzymes. The latter can cause damage or shedding of endothelial cells and increase vascular permeability.

4 The high-permeability of the neocapillary wall The neocapillary buds formed during the repair process have immature endothelial cell connections, which can explain fluid extravasation and edema in recurrent inflammation.

It should be noted that the above four mechanisms all play their roles in the response to certain stimuli. For example, at different stages of thermal injury, fluid extravasation caused by increased vascular permeability can be caused by contraction of endothelial cells caused by chemical mediators, leukocyte-mediated endothelial damage, direct endothelial damage, and permeability of neocapillary wall . Differentiating media may be activated one after another, resulting in sustained reactions.

Local inflammatory edema can dilute toxins and reduce local damage; bring nutrients such as glucose and oxygen to locally infiltrated white blood cells and take away metabolites; antibodies and complements contained in exudate are beneficial for elimination Pathogens; cellulose formed by fibrinogen in the exudate is woven into a network, which can limit the spread of pathogenic microorganisms and limit the lesion on the one hand, and it is also conducive to phagocytic cells to play the role of phagocytosis. The element net can also be used as a scaffold for repair and facilitate the production of collagen fibers by fibroblasts; pathogenic microorganisms and toxins in the exudate are carried to the local lymph nodes with the lymph fluid, which can stimulate the body to produce cellular and humoral immunity.

However, if there is too much exudate, it can affect organ function and compress nearby organs. For example, accumulation of intracellular exudates can affect ventilation, pericardial and pleural effusions can compress the heart, lungs, and severe laryngeal edema can cause suffocation. ,and many more. If the fibrous exudate cannot be completely absorbed, it will become organic. For example, in the lungs, it can cause lung meat quality changes. In the serosal cavity, it can cause serous membrane adhesion and even serous membrane atresia.

Leukocyte exudation and phagocytosis in acute inflammation

The most important function of the inflammatory response is to transport inflammatory cells to the inflammatory site. Leukocyte exudation is the most important feature of the inflammatory response. Exudation of neutrophils and monocytes can engulf and degrade bacteria, immune complexes, and necrotic tissue fragments, forming the main defense link of the inflammatory response. But white blood cells can also cause tissue damage and may prolong the inflammatory process by releasing enzymes, chemical mediators and toxic free radicals.

The exudation process of leukocytes is extremely complicated. It reaches the inflammatory focus through stages such as attachment, adhesion, migration, and chemotaxis, and plays an important defensive role locally.

1. With the expansion of blood vessels, increased vascular permeability and slow blood flow, leukocytes leave the axial flow and roll along the endothelium. At this time, the surface of endothelial cells is lined with a layer of rolling white blood cells, like a crowd moving on the sidewalk. Finally, leukocytes adhere to vascular endothelial cells.

2. Adhesion Although various factors affect the adhesion of endothelial cells and leukocytes, such as the negative charge on the surface of endothelial cells and leukocytes is neutralized and the mutual repulsive force is reduced, and divalent cations bridge endothelial cells and leukocytes to promote adhesion, but this adhesion is now known It is caused by the recognition of endothelial cells and leukocyte surface adhesion molecules (adhesion motecule). Yanping can cause endothelial cells and inflammatory cells to express new adhesion molecules, increase the number of adhesion molecules and enhance affinity with each other.

Some factors act on endothelial cells, while others act on leukocytes, and some act on both, promoting the expression of adhesion molecules.

(1) Expression of leukocyte surface adhesion molecules: Leukocytes increase the expression of three integrin glycoproteins under the action of complement C5a. Integrins are heterodimers composed of different alpha units and beta subunits, and have a wide range of biological functions. Integrins that promote adhesion of leukocytes to endothelial cells and are expressed on leukocytes include LFA-1, MAC-1, and P150-95 (ie, the CD11 / CD18 complex). C5a not only promotes the expression of these three integrins, but also changes its conformation to increase affinity for the ligand.

(2) Expression of adhesion molecules on the surface of endothelial cells: The ligands of MAC-1 and LFA-1 on the surface of endothelial cells are intercellular adhesion molecule 1 (ICAM-1). Under the effect of IL-1 and other inflammatory mediators, endothelial cells can increase the expression of cell surface adhesion molecules. High expression of endothelial leukocyte adhesion molecule 1 (ELAM-1) promotes adhesion of neutrophils; high expression of ICAM-1 promotes adhesion of neutrophils and lymphocytes; vascular cell adhesion molecules (Vascular cell adhesion molecule1, VCAM-1) promotes adhesion of lymphocytes and monocytes.

(3) Tumor necrosis factor (TNF) can promote the expression of endothelial cells and leukocyte adhesion molecules.

3 Evading and chemotaxis The process by which leukocytes enter the surrounding tissue through the vessel wall is called emigration. The white blood cells adhered to the surface of the endothelial cells slowly moved along the surface of the endothelial cells, and the pseudopods protruded at the junction of the endothelial cells. Through the basement membrane to the outside of the blood vessel. This trajectory can be tracked with an electron microscope. It usually takes 2-12 minutes for a white blood cell to completely pass through the vessel wall. Neutrophils, monocytes, lymphocytes, eosinophils, and basophils all swim in this way. Red blood cells can also leak out when the blood vessel wall is severely damaged, but this is a transport process. Hydrostatic pressure pushes red blood cells out of the blood vessels along the path of leukocytes or the endothelial cell necrosis and disintegration.

The leukocytes that swim out are different at different stages of inflammation. In the early stages of acute inflammation, neutrophils migrate first. After 48 hours, mononuclear cell infiltration is the main cause. The reason is that neutrophils have a short life span. After 24 to 48 hours, neutrophils disintegrate and disappear, and monocytes survive for a long time in the tissue. After neutrophils cease to swim, monocytes can continue to swim; the third factor is that different chemokines are activated at different stages of inflammation. It has been confirmed that neutrophils can release monocyte chemokines, so neutrophils will inevitably cause monocytes to migrate. In addition, due to different inflammatory factors, exuded white blood cells are also different: common staphylococcal and streptococcal infections are mainly neutrophil exudation; viral infections are mainly lymphocytes; in some allergic reactions, the Exudation of acid granulocytes is predominant.

Chemotaxis refers to the directional movement of leukocytes towards the location of the chemical stimulus at a speed of about 5 to 20 m per minute. These chemical stimuli are called chemokines. To study the chemotaxis of leukocytes, the trajectory of leukocytes can be recorded using Boyden chamber technology of microporous filter and time-lapse microscopy. Studies have found that the role of chemokines is specific. Some chemokines only attract neutrophils, while others attract monocytes or eosinophils. In addition, different cells respond differently to chemokines. Granulocytes and monocytes respond significantly to chemokines. Lymphocytes respond weakly to chemokines.

Some exogenous and endogenous chemicals have chemotactic effects. Common leukocyte chemokines include soluble bacterial products, components of the complement system (especially C5a), and metabolites of arachidonic acid via the lipid oxygenase pathway (especially leukotriene B4). Monocytes also chemotactic to neutrophil derivatives, factors released by sensitized lymphocytes, and fibronectin fragments. In type I allergies, IgE-sensitized mast cells or basophils can release the allergic reaction eosinophil chemokine (EFC-A) under the stimulation of the same antigen, causing the accumulation of eosinophils . In addition, factors and C5a released by sensitized lymphocytes are also chemokines of eosinophils.

How do white blood cells "discover" chemokines, and how do chemokines cause white blood cells to orient themselves? First of all, there are chemokine receptors on the surface of leukocytes. After a variety of chemokines bind to their specific receptors, they can cause a series of changes in signaling pathway components, although the entire mechanism has not been completely revealed. After activation of chemokines and receptors on the surface of white blood cells, phospholipase C can be activated, resulting in the hydrolysis of phosphatidylinositol 4,5 diphosphate to produce inositol triphosphate and diacetyl glycerol, which in turn increases the free calcium ion in the cell. The first is the release of calcium stored in the cell, and then the extracellular calcium ions enter the cell through the calcium channel. Due to the increase in intracellular calcium ion concentration, intracellular assembly of contractile components that can cause cellular movement. In addition, chemokine binding to the receptor can also activate phospholipase A2, which converts cell membrane phospholipids to arachidonic acid. Diacetyl glycerol plays a role in different stages of leukocyte activation, degranulation, and secretion by activating protein kinase C.

4 The role of white blood cells in the local leukocytes play phagocytosis and immune function in the local area of inflammation, which can effectively kill pathogenic microorganisms, thus becoming an extremely important part of the inflammatory defense response.

(1) Phagocytosis: Phagocytosis refers to the process by which leukocytes swim out to inflammatory foci and swallow pathogens and tissue fragments. There are two main types of phagocytic cells that perform this function; neutrophils and macrophages have basically the same process of phagocytosing foreign bodies, but their structure and chemical composition are different.

1) Types of phagocytes: neutrophils are 10-12 m in diameter, the nucleus is rod-shaped or leaf-like, usually 2 to 5 leaves, chromatin filaments are connected between the leaves, the nuclear chromatin is massive, and the color is dark . The cytoplasm is rich in neutral particles, which is equivalent to lysosomes under the electron microscope. Under the electron microscope, neutral particles can be divided into two types: aniline blue particles and specific particles. The former is also known as azure granules, which have a large volume and high electron density, accounting for about 10% to 20% of all particles. Contains acid hydrolase, neutral protease, myeloperoxidase, cationic protein, lysozyme and phospholipase A2. Specific particles are small and have low electron density, accounting for 80% of all particles. They contain lysozyme, phospholipase A2, lactoferrin, and alkaline phosphatase.

The macrophages in the inflammatory lesions are mostly blood mononuclear cells with a diameter of 14-17 m. The nucleus is kidney-shaped or curved and irregularly folded, and the chromatin particles are thin and loose, so they are lighter in color. The cytoplasm is rich, with lysosomes of inconsistent size, density, and morphology, rich in acid phosphatase and oxidase. Macrophages can be activated by external stimuli, manifesting in increased cell volume, increased cell surface folds, increased mitochondria and lysosomes, and their functions are correspondingly enhanced.

2) Phagocytosis process: including three stages of recognition and adhesion, swallowing and degradation.

Recognition and adhesion: In the absence of serum, it is difficult for phagocytic cells to recognize and engulf bacteria. Because the presence of opsonin in the serum, a type of serum protein that can enhance the phagocytic activity of phagocytes, mainly IgG and C3b. Phagocytic cells can recognize bacteria coated with antibodies or complements through Fc receptors and C3b (C3bi or Mac-1) on the surface of the phagocytic cells. After the antibodies or complements bind to the corresponding receptors, the bacteria are adhered to the surface of the phagocytes.

Swallowing: After the bacteria adhere to the surface of the phagocytic cells, the phagocytic cells protrude from the pseudopods and extend and coincide with each other to form a vesicle body surrounded by phagocytes, called phagosome. The phagosome gradually escapes from the cell membrane and enters the interior of the cell, and fuses with the primary lysosome to form a phagolysosome. The lysosomal contents are poured into it, and the bacteria are killed and degraded in the phagolysosome.

Killing and degradation: The bacteria that enter the phagolysosome are mainly killed by active oxidative metabolites. The phagocytosis dramatically increases the oxygen consumption of white blood cells, which can reach 2 to 20 times the normal consumption, and activates white blood cell oxidase (NADPH oxidase), which oxidizes reduced coenzyme (NADPH) to produce superoxide anion (O2 -).

Most superoxide anions are converted to H2O2 by spontaneous disproportionation. Myeloperoxidase (MPO) is present in neutrophil granulocytes. In the presence of chloride, this enzyme can reduce H2O2 to form hypochlorous acid HOCL.).

HOCL · is a strong oxidant and bactericidal factor. Hydroxyl radicals are another bactericidal factor.

Oxygen metabolites can be sterilized by:

Lipid peroxidation reaction with highly unsaturated fatty acids in phospholipid molecules of bacterial cell membranes, leading to the destruction of the physiological state of cell membranes and the permeability of cell membranes to cations. Increased free calcium ion concentration in bacteria can activate calcium-dependent phospholipases and certain protein kinases, causing damage and death to bacteria.

Redox reactions occur with certain reactive genes on amino acids, proteins and sugar molecules, making enzymes with important physiological functions inactive, and some macromolecular substances change their physical and biological properties.

can pass through the cell membrane to enter the inside of the cell, and interact with the molecules inside the bacteria.

It reacts with bacterial DNA and promotes sister chromatid exchange. In addition, lipid peroxidation produces malondialdehyde during the decomposition process, which cross-links with DNA, which affects DNA replication, blocks bacterial reproduction, and eventually causes bacterial death.

Therefore, the H2O2-MPO-CL- system is the most effective sterilization system, its sterilization efficiency is 50 times stronger than that of H2O2 alone, and it has killing effects on bacteria, fungi, mycoplasma and viruses.

Those oxygen-independent substances in leukocyte granules can also kill pathogens, including increasing bacterial permeability-increasing protein (BPI protein), lysozyme (hydrolyzing the cell wall of cells), lactoferrin, and a new set of findings Arginine-rich cationic protein, which can dissolve bacterial cell walls, is called phagocytin or defensins. After the phagocytosis is completed, the pH of the phagolysosome decreases to 4-5, and the acid hydrolase in it can play a role in degrading bacteria under such a suitable pH environment.

Through the above-mentioned killing effect of phagocytes, most pathogenic microorganisms are killed. However, some bacteria are still in the white blood cells and still have vitality and reproductive power. For example, tuberculosis bacteria, once the resistance of the body declines, these pathogens can reproduce and can spread in the body with the migration of phagocytes. Bacteria living in phagocytic cells are difficult to be affected by antibiotics and the body's defense mechanism, so it is difficult to eliminate them in the body.

(2) Immune response: The immune response requires the coordinated action of lymphocytes, plasma cells, and macrophages. Lymphocytes vary in size, 6 to 16 m in diameter. The nucleus is round or oval, and there is often a small depression on one side of the nucleus. The chromatin of the nucleus is dense and massive, so it is darkly colored. The cytoplasm is small, and a few aniline blue particles without peroxidase can be seen. Lymphocytes are divided into T cells and B cells. Plasma cells have a special shape, with a slightly thick oval shape at one end and a round nucleus, located on the thicker end side of the cell. A heterochromatin with a bright halo nucleus between the cytoplasmic side and the cytoplasm is abundantly arranged in a spoke shape. The cytoplasm is slightly basophilic and is rich in rough endoplasmic reticulum under electron microscope. Its function is to produce antibodies.

After the antigen enters the body, the macrophages phagocytose it, and then present the antigen to T and B cells to sensitize them. Immunely activated lymphocytes produce lymphokines and antibodies, respectively, which play a role in killing pathogenic microorganisms.

Lymphocytic and plasma cell infiltration are common in chronic inflammation, especially chronic granulomatous inflammation associated with cellular immunity, such as tuberculosis and syphilis.

(3) Tissue damage: In some cases, white blood cells can release their products to the extracellular space after activation. These products include lysosomal enzymes, oxygen-derived metabolites, and arachidonic acid metabolites (prostaglandins and leukocytes three). Ene) and so on. These products have a strong role in mediating endothelial cell and tissue damage and aggravating the potency of primitive inflammatory stimulating factors. This leukocyte-mediated tissue damage can be seen in many human inflammatory diseases, and rheumatoid arthritis is an obvious example.

5. Functional Defects of White Blood Cells As mentioned earlier, white blood cells play an extremely important role in the body's defense response. Congenital and acquired leukocyte function defects will cause repeated infections in patients. Cases of congenital dysfunction of white blood cells can deepen the understanding of the role of white blood cells in the inflammatory response. An example is as follows:

(1) Deficiency of phagocytosis: It can be expressed in the entire process from adhesion to endothelial cells to bactericidal activity.

1) Adhesion defects: A typical example is leukocyte adhesion deficiency, which is found in autosomal cryptogenic diseases, and its pathogenesis is due to -chain biosynthetic defects in LFA-1 and Mac-1, which affects leukocyte adhesion to Endothelial cells.

2) Recognition disorders: mainly due to opsonin deficiency, seen in gamma globulin deficiency and complement deficiency.

3) Defects in chemotaxis: It can be manifested as decreased white blood cell motility and obstacles in chemokine production, such as Chédiak-Higashi syndrome (autosomal recessive genetic disease), which is characterized by the presence of giant lysosomes in the cytoplasm of white blood cells. Characteristics, there are a variety of abnormalities, including obstacles to assembly of microtubules, which affect the displacement of white blood cells. Congenital lack of complement hinders chemokine production.

4) Swallowing or degranulation disorders: In Chédiak-Higashi syndrome, due to microtubule assembly failure, the lysosomal contents are poured into the phagosomes and the bactericidal ability of white blood cells is affected. Therefore, the patient presents with repeated purulent infection . Neutrophil actin dysfunction affects the ingestion of pathogens. Of course, the lack of opsonin also affects the ingestion of pathogens.

5) Defective killing effect: H2O2 production disorder is seen in chronic granulomatous disease (CGD). It is an X-linked hereditary disease that affects male infants and children. It is due to the lack of NADPH oxidase, which affects the production of H2O2. H2O2-MPO-CL-sterilization function is poor. Generally, bacteria can produce a small amount of H2O2 during metabolism, but some bacteria can produce catalase that breaks down H2O2, such as Staphylococcus aureus, so the bacteria can survive in patients with CGD. While pneumococcus and other bacteria produce a small amount of H2O2, but do not produce catalase, these H2O2 are enough to start the H2O2-MPO-CL-sterilization function system and kill the bacteria. Therefore, CGD patients often show infection with catalase-positive bacteria. Such cases illustrate the important role of active oxidative metabolites in killing pathogenic microorganisms.

Certain diseases, such as Chédiak-Higashi syndrome and diabetes, affect phagocytosis due to multiple link defects.

(2) Defective immune response: It is mainly a congenital immune deficiency that seriously damages the body's immune function and inflammatory response. Examples include B-cell defects (Bruton syndrome), T-cell defects (Di George syndrome), and immunodeficiency diseases.

Understanding the basic lesions of the acute inflammatory process can clearly shed light on the local manifestations of inflammation. The local small blood vessels in inflammation showed obvious and continuous expansion, causing local tissue to be red. Inflammation that occurs on the body surface or near the skin, due to increased local blood flow, local fever. The main cause of swelling is local edema and accumulation of exudate. The mechanism of local pain is not yet clear, and certain mediators of inflammation such as bradykinin and certain prostaglandins can cause pain. Increased intra-tissue tension due to local edema and exudate accumulation may be the most important factor in pain, so the pain symptoms of abscesses can be immediately relieved after local drainage. Local dysfunction is due to the reflexive inhibition of muscle activity due to pain, and local edema to limit movement.

Acute inflammatory mediator

The mechanisms of vasodilation, increased permeability, and leukocyte exudation in acute inflammatory reactions are important topics in the mechanism of inflammation. Some inflammatory factors can directly damage the endothelium and cause increased vascular permeability, but many inflammatory factors do not directly affect local tissues, but mainly cause inflammation through the action of endogenous chemical factors, so they are also called Chemical or inflammatory mediator.

Inflammatory mediator released by cells

Acute inflammatory vasoactive amines

Includes histamine and serotonin (5-HT). Histamine is mainly found in the granules of mast cells and basophils, and also in platelets. Stimulations that cause mast cells to release histamine include: physical factors such as trauma or heat; immune response, that is, when antigens interact with IgE bound to the surface of mast cells, they can release particles from mast cells; (Anaphylatoxin); neutrophil lysosomal cationic protein; certain neuropeptides. In humans, histamine can dilate the arterioles, shrink the venous endothelial cells, and increase vascular permeability. Histamine can be inactivated by histamine. Histamine also has a chemotactic effect on eosinophils.

5-HT is released by platelets, and collagen and antigen-antibody complexes can stimulate platelet release reactions. Although its effect in rats is similar to histamine, its role in human inflammation is not fully understood.

Acute inflammation arachidonic acid metabolites

Including prostaglandin (PG) and leukotriene (LT), are metabolites of arachidonic acid (AA). AA is a twenty carbon unsaturated fatty acid, which is produced by activating phospholipase under the action of inflammatory stimuli and inflammatory mediators (such as C5a). In inflammation, lysosomes of neutrophils are an important source of phospholipase. AA is metabolized by the cyclooxygenase and lipid oxygenase pathways to produce various products.

In short, inflammation stimulates arachidonic acid metabolism and releases its metabolites, leading to inflammatory reactions such as fever, pain, vasodilation, increased permeability, and leukocyte exudation. On the other hand, anti-inflammatory drugs such as aspirin, indomethacin and steroid hormones can inhibit arachidonic acid metabolism and reduce the inflammatory response.

Acute inflammatory leukocyte product

After being activated by inflammatory factors, neutrophils and monocytes can release oxygen free radicals and lysosomal enzymes, promote inflammatory reactions and destroy tissues, becoming inflammatory mediators.

1) Active oxygen metabolites: Its effects include three aspects: Damage to vascular endothelial cells leads to increased vascular permeability. Inactivation of anti-protease (such as inactivating 1 antitrypsin), resulting in increased protease activity, which can destroy tissue structural components, such as elastic fibers. damage red blood cells or other parenchymal cells.

Of course, serum, interstitial fluid, and target cells also have antioxidant protection mechanisms, so whether they cause damage depends on the balance between the two.

2) Lysosomal components of neutrophils: Due to the death of neutrophils, efflux and effusion during the formation of phagocytic vesicles, lysosomal components can be released externally and mediate acute inflammation. Among them, neutrophil proteases such as elastase, collagenase and cathepsin can mediate tissue damage.

Cationic proteins have the following biological activities: causing mast cells to degranulate and increasing vascular permeability; chemotactic effects on monocytes; acting as neutral and eosinophil migration inhibitory factors.

Acute inflammatory cytokines

Cytokines are mainly produced by activated lymphocytes and monocytes, which can regulate the functions of other cell types, play an important role in cellular immune responses, and also have important functions in mediating inflammatory responses.

The secretion of IL-1 and TNF can be stimulated by a variety of inflammatory factors such as endotoxin, immune complexes, physical damage, etc., and can act through autocrine, paracrine, and systemic effects. In particular, they can promote the expression of adhesion molecules by endothelial cells and increase the adhesion of leukocytes to them. Fever can also cause acute inflammation. TNF can also promote neutrophil aggregation and activate interstitial tissue to release proteolytic enzymes. IL-8 is a powerful chemokine and activator of neutrophils.

Acute inflammatory platelet activating factor

Platelet activating factor (PAF) is another inflammatory mediator of phospholipid origin. It is produced by IgE-sensitized basophils after binding to antigen. In addition to activating platelets, PAF can increase blood vessel permeability, promote white blood cell focus and adhesion, and chemotaxis. In addition, it has the function of affecting the whole body hemodynamics. Basophils, neutrophils, monocytes, and endothelial cells all release PAF. On the one hand, PAF can directly act on target cells and stimulate cells to synthesize other inflammatory mediators, especially PG and leukotriene.

Acute inflammation other inflammatory mediators

Substance P can directly and indirectly stimulate mast cell degranulation and cause vasodilation and increased permeability. Nitric oxide produced by endothelial cells, macrophages and other cells can cause vasodilation and cytotoxicity.

2. Inflammatory mediators produced in body fluids There are three interrelated systems in plasma, namely kallikrein, complement and the coagulation system; important inflammatory mediators.

(1) Kinin system: Activation of the kallikrein system eventually produces bradykinin, which can cause arteriolar dilatation, endothelial cell contraction, increased fine vein permeability, and contraction of smooth muscles other than blood vessels. Bradykinin is quickly inactivated by plasma and tissue kininase, and its effect is mainly limited to the early stage of increased vascular permeability.

(2) Complement system; Complement system is composed of a series of proteins. There are two ways to activate complement-classical and alternative pathways. In the complex environment of acute inflammation, the following factors can activate complement: The antigenic component of pathogenic microorganisms and antibodies activate complement via classical pathways, while endotoxin of Gram-negative bacteria activates complement via alternative pathways. In addition, certain bacteria produce enzymes that can also activate C3 and C5. Enzymes released by necrotic tissue can activate C3 and C5. The activation of kinin and fibrin formation and degradation systems and their products can also activate complement.

Complement can affect acute inflammation from the following three aspects: C3a and C5a (also known as allergic toxins) increase the permeability of blood vessels and cause vasodilation, all by causing mast cells and monocytes to further release inflammatory mediators; C5a can also activate The lipid-oxygenase pathway of arachidonic acid metabolism makes neutrophils and monocytes further release inflammatory mediators; C5a causes neutrophils to adhere to vascular endothelial cells, and is neutrophil and monocytes. Chemokines; C3b has an opsonin effect when bound to the bacterial cell wall, which can strengthen the phagocytic activity of neutrophils and monocytes, because there are C3b receptors on the surface of these phagocytic cells.

C3 and C5 are the most important mediators of inflammation. In addition to the aforementioned activation pathways, C3 and C5 can also be activated by proteolytic enzymes, including plasmin and lysosomal enzymes, that are present in inflammatory exudates. As a result, an endless loop of neutrophils is formed, that is, complement has chemotactic effects on neutrophils, and lysosomes released by neutrophils can activate complement.

(3) The coagulation system: factor activation can not only activate the kinin system, but also start the two systems of blood coagulation and fibrinolysis. Thrombin releases fibrin polypeptide in the process of converting fibrinogen to fibrin, which can increase vascular permeability and is a chemokine for leukocytes.

The fibrinolytic system can cause inflammatory vascular changes through the kallikrein system. Plasminogen activating factor produced by endothelial cells, leukocytes and other tissues can transform plasminogen into plasmin, which affects the process of inflammation through the following three reactions: activation of factor Start the process of bradykinin generation; C3 cleavage produces C3 fragments; degradation of fibrin produces its lysate, which in turn increases vascular permeability.

There are two points worth noting about the role of inflammatory mediators. First, different media systems are closely related to each other. For example, the close relationship between the activation of the complement, kallikrein, coagulation system, and fibrinolytic system and their products is illustrated in Figure 5-8. The effects of these inflammatory mediators are also intertwined. Second, almost all media are in a sensitive regulation and balance system. On the one hand, the medium that is tightly isolated in the cell or the precursor that is in the plasma and tissue must undergo many steps to be activated. During its transformation, the rate-limiting mechanism controls the biochemical response of the medium speed. On the other hand, once the medium is activated and released, it will be quickly inactivated or destroyed. It is through this regulatory system that the body makes the media in a dynamic equilibrium.

Types of acute inflammation

Due to the different inflammatory factors, the severity of the tissue response and the location of the inflammation, the pathological morphology of acute inflammation is also different. According to the main components of exudates, acute inflammation is divided into serous inflammation, fibrous inflammation, suppurative inflammation, and hemorrhagic inflammation.

Acute inflammation serous inflammation

Serous inflammation is characterized by serum exudation. The main component of exudation is serous fluid, which is mixed with a small amount of white blood cells and cellulose. The serum contains 3% to 5% protein, mainly albumin. Serous inflammation often occurs in loose connective tissue, serosa, and mucosa. Serous exudate infiltrated into the tissue diffusely, and obvious inflammatory edema appeared locally, such as the poisonous snake bite and second-degree burn on the skin, and the exudate accumulated in the epidermis, forming a blister. Serum inflammation in the body cavity causes inflammatory effusion, not only from exudation of blood vessels, but also from increased secretion of mesothelial cells, such as tuberculous pleurisy and rheumatoid arthritis. Mucosal serous inflammation is also called serous catarrh, such as rhinitis seen in the early stages of a cold. The word catarrh comes from the Greek word, which means trickle down. Generally used for exudative inflammation of the mucous membrane, which describes that there is more exudate, which is discharged outward along the mucosal surface. In serosal or mucosal serous inflammation, mesothelial or epithelial cells can undergo degeneration, necrosis, and shedding.

Serous inflammation is generally mild and easily subsides. However, sometimes the excessive exudation of serous fluid can lead to serious consequences. For example, when there is a large amount of serous fluid in the thoracic cavity and pericardial cavity, it can affect breathing and cardiac function.

Acute inflammation

Fibrinous inflammation is mainly caused by fibrinogen exudation and formation of cellulose in the inflammation focus. Under light microscopy, hematoxylin and eosin staining showed a large number of red-stained cellulose intertwined in a network, and the neutrophils and necrotic cell debris were present in the gap. Large pieces of cellulose appear as flakes, red stains, and uniform texture under the microscope. The large amount of fibrinogen exudates, indicating that the vessel wall is severely damaged, mostly due to certain bacterial toxins (such as toxins of diphtheria, dysentery, and pneumococcus) or various endogenous or exogenous toxic substances (such as uremia Caused by urea and mercury poisoning). Lesions often occur in the mucosa, serosa, and lungs. In fibrous inflammation of the mucosa (such as diphtheria, bacterial dysentery), cellulose, white blood cells and necrotic mucosal epithelium are often mixed together to form a gray-white film called a pseudomembranous membrane. Therefore, the fibrous inflammation of the mucous membrane is also called pseudomembranitis. Due to the different characteristics of the local tissue structure, some false membranes are firmly attached to the mucosal surface and are not easy to fall off (such as diphtheria), while some false membranes are loosely connected to the damaged part of the mucosa and easily fall off (such as trachea diphtheria). Suffocation due to blocked bronchi. Cellulitis of the serosa is common in the pleural and pericardial cavities, such as fibrinous pleurisy and rheumatic pericarditis caused by Pneumococcus pneumoniae. In the pericardial fibrous inflammation, due to the beating of the heart, the cellulose on the epicardium forms countless villi and covers the surface of the heart, so it is also called "villed heart". In addition, a large amount of fibrinogen exuded during the red and gray liver-like metamorphosis of lobar pneumonia.

A small amount of cellulose can be solubilized and absorbed by lysin released by neutrophils. However, normal serum and tissues contain a certain amount of antitrypsin, which counteracts the effects of neutrophil to a certain extent. Therefore, if there is more cellulose and less lysoprotease released by neutrophils or more antitrypsin in the tissue, the cellulose cannot be completely dissolved and absorbed, resulting in the organization of the plasma membrane. Thickening and adhesions, or even atresia of the serous cavity, seriously affects organ function.

Acute inflammatory purulent inflammation

Suppurative or purulent inflammation is characterized by massive exudation of neutrophils, accompanied by varying degrees of tissue necrosis and pus formation. Mostly caused by staphylococci, streptococcus, meningococcus, Escherichia coli and other pyogenic bacteria, but also caused by certain chemicals (such as turpentine) and the body's necrotic tissue. The clinically common purulent inflammations include , , pyogenic appendicitis, and pyogenic meningitis. Purulent exudate, called pus, is a turbid curd-like liquid with a grayish yellow or yellowish green color. The pus caused by staphylococcus is dense, while the pus caused by streptococcus is thinner. Except for a few neutrophils that can still maintain their phagocytosis ability, most of the neutrophils have undergone degeneration and necrosis, that is, they become pus cells. In addition to pus cells, the pus also contains bacteria, lysate of necrotic tissue, and a small amount of serum. Purulent inflammation can be divided into the following three categories according to the cause and location of purulent inflammation.

(1) Surface suppuration and empyema: Surface suppuration refers to suppurative inflammation of the serosa or mucosal tissue. Mucosal purulent inflammation is also called purulent catarrh. At this time, the neutrophils mainly exuded to the mucosal surface, and there was no obvious inflammatory cell infiltration in deep tissues, such as purulent urethritis or purulent bronchitis. The exuded pus can be discharged through the urethra and trachea. When this lesion occurs in the serosa or the mucosa of the gallbladder and fallopian tubes, pus accumulates in the serosa or in the gallbladder and fallopian tubes, called empyema.

(2) Cellulitis (phlegmonous inflammation): Chronic suppuration in loose tissue is called cellulitis, which is common in the skin, muscles and appendix. Cellulitis is mainly caused by hemolytic streptococci. Streptococcus can secrete hyaluronidase and degrade hyaluronic acid in connective tissue matrix; it secretes streptokinase and dissolves cellulose. As a result, bacteria are prone to diffuse infiltration through the interstitial space and the spread of lymphatic vessels.

(3) Abscess: It is a localized suppurative inflammation, which is mainly characterized by necrosis and dissolution of tissues, forming a cavity filled with pus, which is called an abscess. Can occur under the skin or internal organs, often caused by Staphylococcus aureus. These bacteria can produce toxins to cause local tissue necrosis, followed by a large number of neutrophil infiltration. Later, granulocyte collapse explains that the enzyme liquefies the necrotic tissue and forms a cavity containing pus.

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hemorrhagic inflammation

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(3) Septicemia: Severely toxic bacteria enter the blood not only are not cleared, they also multiply, and produce toxins, causing systemic symptoms and pathological changes, called sepsis. In addition to the clinical manifestations of severe toxemia, patients often have multiple bleeding spots on the skin and mucous membranes and spleen and systemic lymphadenopathy. At this time, pathogenic bacteria can often be cultured in the blood.

(4) sepsis (pyemia): sepsis caused by pyogenic bacteria can further develop into sepsis. At this time, in addition to the symptoms of sepsis, multiple abscesses were also formed in some organs (such as lung, kidney, liver, etc.). These abscesses are usually smaller and more evenly spread throughout the organ. Under the microscope, bacterial colonies are common in the center of the abscess and the remaining capillaries or small blood vessels, indicating that the abscess is caused by pyogenic bacteria embolized in the capillaries of the organ, so it is called embolic abscess or metastatic abscess (Metastatic abscess).

Acute inflammation treatment technology

Acute inflammation light energy detoxification technology

Technical overview:

Pelvic inflammatory disease light energy detoxification therapy is specifically targeted at pelvic inflammatory disease treatment. It has powerful functions of sterilizing, removing necrotic cells and toxins, clearing the metabolic environment, and improving the body's immunity. It is the first country in China to realize the "two-way detoxification of the pelvic area and blood as a whole. Inflammation "purpose. ^[1]

First, pelvic detoxification treatment. This therapy introduces effective Chinese and western medicines with blood circulation, blood stasis and detoxification effects into the pelvic cavity through ion nebulizer introduction technology, kills and removes viruses in the pelvic cavity, controls the aggravation of inflammation, effectively eliminates inflammation and analgesics, and realizes pelvic detoxification treatment.

Secondly, blood light energy detoxification treatment. The intelligent external short-wave ion electric field treatment system is used to directly remove the viruses in the blood circulation system in a three-pronged way by using the unique optical energy, magnetic effects, and thermal effects in the form of ions to complete the blood circulation detoxification treatment.

Finally, comprehensive consolidation treatment. It is supplemented with effective antibiotics and ecological immunomodulatory drugs for oral or infusion consolidation treatment to quickly kill residual pathogens, improve the body's immunity, and restore ecological balance.

Acute inflammation common types of gynecological inflammation

Acute inflammation vaginitis

More and more women are susceptible to vaginitis, and there is no age limit for the affected population, and a few young girls will also develop symptoms of vaginitis. Vaginitis is one of the common gynecological inflammations. Due to the complexity and diversity of social lifestyles, some young women even suspect that they have a sexually transmitted disease, but are ashamed to open their teeth and dare not go to a regular hospital for gynecology, resulting in delays.

Acute inflammation cervicitis

Cervicitis is a common disease of women of childbearing age, especially middle-aged women. Mechanical irritation or damage, microorganisms and their toxins, chemicals, and radiation can all be the cause of cervicitis. The main symptoms are increased vaginal discharge, lumbosacral pain, pelvic sensation and dysmenorrhea, infertility and cervical erosion.

Acute inflammation urethritis

Urethritis is a common disease, which is more common in women. The most common pathogenic bacteria are Escherichia coli, Streptococcus and Staphylococcus. In most cases, symptoms of urinary tract irritation are obvious, with or without sterile urine. The number of white blood cells in the urine sediment was> 5 per high power field. The main symptoms are frequent urinary urgency and dysuria, which have greatly affected patients' lives.

Acute inflammation pelvic inflammatory disease

Acute and chronic inflammation of the internal genital organs and the surrounding connective tissue and pelvic peritoneum is called pelvic inflammatory disease. It is a common gynecological disease, and inflammation can be confined to one site or several sites at the same time. Its main symptoms are lower abdominal pain and fever. If the condition is severe, there may be high fever, chills, headache, and loss of appetite.