What are the main functions of inflammatory mediators?

People usually hear about various inflammatory diseases, such as gynecological inflammation, lung inflammation, digestive tract inflammation, skin inflammation, etc. In fact, when inflammation occurs in the human body, the body will have a series of reactions, which cause symptoms such as itching and pain. In this process, inflammatory mediators play an important role. The following is a detailed introduction to the role and efficacy of inflammatory mediators.

The main effects of inflammatory mediators are:

There are two points worth noting about the role of inflammatory mediators.

Different media systems are closely related to each other

Complement, kinins, and the activation of the coagulation and fibrinolytic systems and their products are closely related, and the effects of these inflammatory mediators are also intertwined.

Almost all media are in a sensitive regulation and balance system

On the one hand, mediators that are in a state of strict isolation within cells, or in a precursor state in plasma and tissues, must go through many steps before they can be activated. During their conversion process, rate-limiting mechanisms control the speed of the biochemical reactions that produce the mediators. On the other hand, once activated and released, mediators are rapidly inactivated or destroyed. The body uses this regulatory system to keep the body's media in dynamic balance.

Vasoactive amines

Including histamine and 5-hydroxytryptamine (5-HT). Histamine is mainly present in the granules of mast cells and alkaliphils, and is also present in platelets. Stimuli that cause mast cells to release histamine include: ① physical factors such as trauma or heat; ② immune response, that is, when antigens interact with IgE bound to the surface of mast cells, mast cells can release granules; ③ complement fragments, such as anaphylatoxin; ④ neutrophil lysosomal cationic proteins; ⑤ certain neuropeptides. In humans, histamine can dilate arterioles and constrict venular endothelial cells, leading to increased vascular permeability. Histamine can be inactivated by histaminase. Histamine also has a chemotactic effect on eosinophils.

5-HT is released by platelets, and collagen and antigen-antibody complexes can stimulate platelets to release response. Although its effects in rats are similar to those of histamine, its role in human inflammation is not well understood.

Arachidonic acid metabolites

Including prostaglandins (PG) and leukotriene (LT), both are metabolites of arachidonic acid (AA). AA is an 20-carbon unsaturated fatty acid that is produced by activating phospholipase under the action of inflammatory stimulation and inflammatory mediators (such as C5a). In inflammation, the lysosomes of neutrophils are an important source of phospholipase. AA is metabolized via the cyclooxygenase and lipid oxygenase pathways to produce various products.

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

Leukocyte products

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

1) Reactive oxygen metabolites: Its effects include three aspects: ① Damage to vascular endothelial cells leading to increased vascular permeability. ② Inactivate antiproteases (such as α1 antitrypsin), resulting in increased protease activity, which can destroy tissue structural components such as elastic fibers. ③ Damage to red blood cells or other parenchymal cells.

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

2) Neutrophil lysosomal components: Due to the death of neutrophils, overflow during phagocytic vacuoles formation and exocytosis, lysosomal components can be released 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: ① causing mast cell degranulation and increasing vascular permeability; ② having a chemotactic effect on monocytes; ③ acting as a neutrophil and eosinophil migration inhibitory factor.