What Is Chronic Inflammation?

Damage factors can be the cause of inflammation. Although there are many types of inflammatory factors, they can be grouped into the following categories.

Chronic inflammation

The persistence of inflammatory factors and tissue damage is the root cause of chronic inflammation. Chronic inflammation of various organs, in addition to being transformed from acute inflammation, can also occur in other ways. Acute inflammation recurs repeatedly, and there are no obvious symptoms during the episode, but also chronic inflammation, such as chronic cholecystitis and chronic pyelonephritis. Chronic inflammation can also occur slowly and gradually. There is no acute inflammation in the clinic. It is common in intracellular infections (such as Mycobacterium tuberculosis and viral infections). These pathogens are not toxic, but they can cause immune responses; Stimulation by non-degradable but potentially toxic substances (such as silicosis); or persistent immune responses against self-tissues, ie autoimmune diseases (such as rheumatoid arthritis).

Chinese name

Chronic inflammation

Foreign name

Chronic inflammation

root cause

Proinflammatory factors persist and damage tissue

Clinical manifestation

Intracellular infection

Causes of chronic inflammation

Chronic inflammation

Damage factors can be the cause of inflammation. Although there are many types of inflammatory factors, they can be grouped into the following categories.

Physical cause

Chronic inflammation , high fever,

Low temperature, radiation and ultraviolet.

Chronic inflammation

2. Chemical factors include exogenous and endogenous chemicals. Exogenous chemicals include corrosive substances such as strong acids and alkalis, turpentine, mustard gas, etc. Endogenous chemical poisons such as the decomposition products of necrotic tissue and metabolites such as urea accumulated in the body under certain pathological conditions.

3. Mechanical factors such as cutting, impact, extrusion, etc.

4. Biological factors Bacteria, viruses, Rickettsia, Mycoplasma, fungi, Borrelia and parasites are the most common causes of inflammation. They multiply in the body, produce and release toxins that directly cause cell and tissue damage, and can also induce inflammation through their antigenicity.

5. Immune reactions All types of allergies can cause tissue and cell damage and cause inflammation: type allergies such as allergic rhinitis and urticaria; type allergies such as anti-basal membrane glomerulonephritis; type allergies Such as immune complex glomerulonephritis and type IV allergies such as tuberculosis, typhoid fever, etc .; In addition, there are certain autoimmune diseases such as lymphocytic thyroiditis, ulcerative colitis and so on.

Whether the damage factors cause the body to cause inflammation, and the strength of the inflammatory response is not only related to the nature of the damage factors and the intensity of the damage, but also to the body's sensitivity to the damage factors, such as the immune function of young children and the elderly is susceptible Pneumonia is also more serious; children who have been vaccinated against vaccination often show insensitivity to the pathogen. Therefore, the occurrence and development of inflammatory response depend on the combined effects of damage factors and body reactivity.

Chronic inflammation Basic pathological changes of chronic inflammation

The basic pathological changes of the disease include local tissue alteration, exudation, and proliferation. During the inflammatory process, these pathological changes occur in a certain sequence. Generally, metamorphosis and exudation are the main changes in the early stage. In the later period, mainly hyperplasia, but the three

Chronic inflammation is closely related to each other

Department. Generally speaking, metamorphism belongs to injury process, while exudation and proliferation belong to anti-damage process.

Chronic inflammation

1. The degeneration and necrosis of the local tissue of metamorphic inflammation is called metamorphism. Metamorphosis can occur in both parenchymal cells and mesenchymal cells. Degeneration of parenchymal cells often includes cell edema, steatosis, coagulation or liquefaction necrosis. The deterioration of interstitial connective tissue can manifest as mucus degeneration, cellulose-like degeneration or necrosis. Pro-inflammatory

Direct injury of chronic inflammation , during inflammation

The combined effects of the impaired blood circulation and the inflammatory response products cause the deterioration of local tissues. Therefore, the severity of metamorphism is determined by two aspects of inflammatory factors and body response.

2. The process of exuding fluids, proteins, and blood cells in the blood vessels of inflammation local tissues through the blood vessel wall into the interstitial space, rest space, body surface or mucosal surface is called exudation. Exudative lesions centered on vascular response are important signs of inflammation and have important defensive effects locally. Inflammation exudation is caused by increased local vascular permeability and active effusion of leukocytes. The inflammatory exudate has a higher protein content and contains more cellular components and debris. Therefore, the exudate of the serosal cavity caused by inflammation has a specific gravity higher than 1.020, an appearance that is erosive, and a large amount of cells, which are different from the transudate that is simply caused by the blocked venous return. Exudate and leakage can accumulate in the interstitial tissue, causing edema, or hydrops in the serosal cavity.

3 Proliferation Macrophages, endothelial cells and fibroblasts can proliferate under the stimulation of inflammatory factors, tissue disintegration products or certain physical and chemical factors. Local epithelial or parenchymal cells can also proliferate in some cases. It is this proliferative response that repairs damaged tissue. Many growth factors are involved in stimulating the proliferation of interstitial and parenchymal cells in a mechanism similar to that of regeneration and repair.

4 Macrophages, lymphocytes, and plasma cells infiltrate the inflammatory focus. Infiltration of monocyte phagocytes is important for chronic inflammation. Monocytes are transformed into macrophages after they escape from the blood vessels. Macrophages can also be activated. There are three reasons for the accumulation of local macrophages in inflammatory foci: As chemokines attracting monocytes are continuously produced from inflammatory foci, such as C5a, fibrin peptides, cationic proteins, and decomposition products of collagen and fibronectin. Therefore, the mononuclear cells exuding from the blood circulation continuously come to the local area, which is the main source of local macrophages. The macrophages that swim out proliferate locally through mitosis, but the initial cause of local macrophage proliferation is unclear. The macrophages in the inflammatory lesions have a long life span and can stay in place for a long time without swimming. Monocytes can be activated by factors such as cytokines (such as interferon gamma), bacterial endotoxins, and contact with fibronectin-coated interfaces. Activated monocytes secrete a variety of biologically active products and are important mediators of tissue destruction and fibrosis in chronic inflammation.

Chronic inflammation

As for the role of lymphocytes and plasma cells in immune-related inflammatory responses, their functions in non-immune inflammation have yet to be studied. It should be noted that neutrophils are usually a sign of acute inflammation, but in some chronic inflammations, a large number of neutrophil infiltration can also be seen, and pus can be formed; conversely, lymphocyte infiltration is not always a characteristic of chronic inflammation. In acute viral infections such as acute viral hepatitis, lymphocytes are a major component of inflammatory infiltration. Cytokines produced by monocytes can activate lymphocytes, and activated lymphocytes can produce inflammatory mediators, which is also an important factor that causes chronic inflammation to persist. Eosinophils are very common in IgE-mediated immune responses and parasitic infections. The major basic protein (MBP) contained in the particles is toxic to the parasites and can cause lysis of mammalian epithelial cells. .

5. Fibroblasts proliferate and sometimes small blood vessels proliferate. The mechanism of these changes in chronic inflammation is still being studied, but some mediators may play a role. In vitro experiments show that platelet-derived growth factor (PDGF) and fibronectin (FN) decomposition products have chemotactic effects on fibroblasts. In addition, platelet-derived growth factors, macrophages, and lymphocyte-derived factors can stimulate fibroblast proliferation and produce large amounts of collagen in vitro. Therefore, chronic inflammatory reactions are often accompanied by obvious scar formation, causing intestinal stenosis and serosal surface adhesion. Macrophage-derived soluble factors can stimulate angiogenesis in vivo.

6. Some special components of local tissues, such as the covered epithelium, glandular epithelium, and other parenchymal cells of inflammatory lesions, can also undergo significant proliferation.

Chronic inflammation chronic granulomatous inflammation

Chronic inflammation, characterized by the formation of clear nodular lesions mainly composed of macrophage hyperplasia, is called chronic granulomatous inflammation. The nodules are small with a diameter of 0.5 to 2 mm. This is a special type of chronic inflammation. Different etiologies can cause different forms of granulomas, so pathology can make a diagnosis based on the typical morphological characteristics of granulomas. If you see the morphological structure of tuberculous granulomas (tubercular nodules), you can diagnose tuberculosis.

Common causes of chronic inflammation of chronic granulomatous inflammation

(1) Some classic examples of bacterial infections are tuberculosis, leprosy and prune.

(2) Fungal and parasitic infections, such as histoplasmosis and schistosomiasis.

(3) Foreign objects, such as surgical sutures, asbestos and talcum powder.

(4) The cause is unknown, such as sarcoidosis.

Conditions for chronic inflammation to form granulomas

(1) Pathogens (such as Mycobacterium tuberculosis) or foreign bodies (mineral oil) cannot be digested, stimulating long-term existence and causing chronic inflammation.

Chronic inflammation

(2) Experiments have shown that the cell-mediated immune response caused by stimuli plays an important role in inducing chronic granulomatous inflammation. In vitro experiments confirmed that the T cell product, lymphokine, can enhance the transformation of monocytes to multinucleated giant cells.

Composition of chronic inflammatory granulomas

The composition of granulomas is based on tuberculosis nodules. From the center of the nodule, the components of the granulomatosis are:

(1) Caseous necrosis: The center of a typical tuberculosis nodule is caseous necrosis, which contains necrotic tissue cells and white blood cells, as well as tubercle bacilli. Necrosis at the center of tuberculosis nodules may be the result of a cell-mediated immune response.

(2) epithelioid cells: A large number of cells with large cell bodies and unclear boundaries can be seen around the caseous necrosis. The nucleus of these cells is round or oval, with less chromatin, and may even be vacuolated. The nucleus may have 1 or 2 nucleoli, and the cytoplasm is rich and stained light red. According to its morphology similar to epithelial cells, it is called epithelial-like cells.

It is now believed that, under the long-term stimulation of some indigestible bacteria or other antigenic substances, macrophages can be transformed into epithelial cells and undergo drastic changes: the increase of chromatin in the nucleus, indicating DNA activation; The increase of nucleoli near the nuclear membrane indicates that rRNA synthesis is enhanced. The cytoplasm is rich in endoplasmic reticulum, ribosome, Golgi apparatus, and various vacuoles, which indicate that the synthesis of organelles and enzymes is enhanced and active secretion; Mitochondria, slippery The endoplasmic reticulum and lysosomal components were significantly increased, so the cytoplasmic components expanded, and the cells were arranged closely like epithelial cells; The Fc receptor and C3b receptor of the cell membrane were greatly reduced, and the phagocytosis function was significantly reduced. It seems that epithelioid cells have the function of secreting extracellularly, not phagocytosis.

The function of the transformed epithelial cells is not clear. But they may kill bacteria around the cells by secreting some chemicals; at the same time, they form an isolation zone between the host's healthy tissue and the bacteria. Macrophages do not transform into epithelial cells during the process of phagocytosing foreign bodies. If too many macrophages enter the inflammatory focus, they may transform into epithelial cells.

(3) Multinucleated giant cells. Multinucleated giant cells are scattered between epithelioid cells. Multinucleated giant cells of tuberculous nodules are also called Langhans giant cells. Such giant cells are very large, with a diameter of 40-50 m. The nucleus has a similar morphology to epithelial-like cells, with a number of up to tens, or even more than a hundred, arranged in a horseshoe or ring shape around the periphery of the cell, with abundant cytoplasm. The Langhans giant cell line is formed by the fusion of epithelial-like cells; epithelial-like cells first protrude from the cytoplasmic protrusions, then the cell bodies approach each other, and finally the fusion of the cytoplasmic protrusions causes the epithelial-like cells to fuse together to form multinucleated giant cells. But the mechanism of fusion remains to be seen.

Chronic inflammation

Multinucleated giant cells are also commonly found around large foreign bodies that are not easily digested (such as surgical sutures, asbestos fibers, etc.) and metabolites (such as urate crystals of gout). Many macrophages surround the stimulus and fuse with each other to form giant phagosomes surrounded by the plasma membrane of most macrophages. Nuclei are scattered in the cytoplasm of the giant cells. Such multinucleated giant cells are called foreign body giant cells and are more common in chronic granulomatous inflammation caused by foreign body stimulation.

Multinucleated giant cells move very slowly, at about 0.04 to 1 m per minute, and move more slowly as the number of nuclei increases. After macrophages are fused into multinucleated giant cells, the number of Fc and C3b receptors on their membranes is also greatly reduced. Therefore, multinucleated giant cells function similarly to epithelial-like cells, and may secrete some substances that kill biological pathogens and participate in the formation of a barrier structure that isolates host tissues from bacteria.

Both epithelial-like cells and multinucleated giant cells are derived from macrophages. If the occurrence of chronic granulomatous inflammation is related to cell-mediated immunity, the local concentration of macrophages is also related to the lymphokine-macrophage chemotactic factor (MCF) and macrophage migration inhibitory factor secreted by activated T cells. (MIF). And these macrophages are also affected by macrophage activating factor (MAF), which increases their phagocytic activity.

(4) Lymphocytes: A large number of lymphocyte infiltration can be seen around epithelial-like cells.

(5) Fibroblasts: Fibroblasts and collagen fibers are distributed around tuberculous nodules.

In addition to general and specific manifestations of chronic inflammation, inflammatory polyps and inflammatory pseudotumors can sometimes form. Inflammatory polyp (inflammatory polyp) is a proliferative granuloma on the mucosal surface formed by the proliferation of local mucosal epithelium and glands and granulation tissue under the long-term stimulation of inflammatory factors. It is common in the nasal mucosa and cervix. An inflammatory pseudotumor is a well-defined tumor-like mass formed by inflammatory hyperplasia of tissues, which often occurs in the orbit and lungs.

Non-specific chronic inflammation

Non-specific chronic inflammation, the lesions are mainly fibroblasts, vascular endothelial cells and histiocytosis, accompanied by lymphocytes, plasma cells

Chronic inflammation

Infiltration of chronic inflammatory cells such as macrophages, and localized epithelial, glandular epithelial, and parenchymal cells can also proliferate.

Chronic inflammation other

Chronic inflammation can also be accompanied by granulation tissue formation. This type of inflammation is often associated with large tissue defects. At this time, granulation tissue plays an important role in the absorption and decomposition of chronic abscesses, fistulas, and chronic mucosal ulcers.

Chronic inflammation chronic inflammation book

Basic information about chronic inflammation

Book title: Chronic inflammation

Author :( day) Ikuta Zhe

Publisher: World Book Publishing Company

Published: 2007

ISBN: 9787506288712

Folio: 32

Price: 22.80 RMB

Introduction to chronic inflammation

This series of books uses in-depth language and vivid illustrations to introduce the latest interpretation of life in modern science and the understanding of common diseases, including genes and inheritance, development and aging, infection and immunity, human body structure and function The latest knowledge helps people who love life and pursue health to learn more about their bodies, understand the various factors that affect health, and provide a guarantee of knowledge for the pursuit of a healthy life.

Chronic inflammation catalog

Chapter 1 Inflammation, the cause of heart disease, diabetes, cancer, and senile dementia

1. Lifestyle diseases are caused by chronic inflammation

2. Acute inflammation and chronic inflammation

3. Newly discovered shocks in chronic inflammation

4. Sharp increase in patients with chronic diseases

5. Why are inflammatory diseases so serious

...