What is the Mechanism of Acute Inflammation?

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The body has the capacity to respond to both minor injuries such as bruising, scratching, cuts, and abrasions, as well as to major injuries such as severe burns and amputation of limbs through inflammation.

Inflammation initiates a series of catabolic and anabolic processes that occur in a defined order to re establish homeostasis.

The body responds to injury by healing and repairing the damaged tissue, as well as by eliminating the infectious agents and their toxins that might have entered the wound.

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When there is any damage to living tissues, inflammatory response begins in a cascade fasion.

The factors that can stimulate inflammation include microorganisms, physical agents, chemicals, tissue death, and inappropriate immunological responses also.

The events that occur in inflammation are:

(1) The activation of resident cells (mast cells, resident macrophages and dendrite cells) and rapid entry of granulocytes in response to injury,

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(2) Further recruitment of macrophages,

(3) Infiltration of effectors immune cells (lymphocytes) to enable specific immune responses,

(4) Recruitment and activation of mesenchymal cells such as endothelial cells and fibroblasts to form new blood vessels and a collagenous matrix; and (5) tissue remodelling.

In its initial stages, inflammation is an aggressive state that can destroy both exogenous pathogens and host tissues. This is followed by a switch to a state that promotes cell survival and tissue regeneration.

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Factors associated with tissue damage trigger inflammation, the sequence of changes are as follows:

1. Release of Chemical Mediators:

Although injury starts the inflammatory response, chemical factors released upon this stimulation bring about the vascular and cellular changes, necessary for inflammation.

Most of the mediators involved in inflammation originate from blood plasma, white blood cells (basophils, neutrophils, monocytes, and macrophages), platelets, mast cells, endothelial cells lining the blood vessels, and damaged tissue cells.

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Histamine is one of the best-known chemical mediators released from cells during inflammation. In the presence of the foreign substance or injury phagocytes of surrounding area especially mast cells liberate cytokines, lipid messengers, and various other mediators of inflammation.

Mast cells found throughout the body are filled with large vesicles containing histamine and other inflammatory paracrines. When these cells are stimulated, histamine stored in the form of vesicles in mast cells is released immediately into the surroundings, along with other substances such as, prostaglandin D2 (PG D2) , several Leucotrines (Ts) and TNFa.

Histamine triggers vasodilation and increases vascular permeability. Many cytokines secreted by cells involved in inflammation also have vasoactive and chemotactic properties.

Prostaglandins a group of fatty acids produced by many types of cells at the site of injury are associated with the pain and fever in inflammation. Some prostaglandins increase the effects of other substances that promote vascular permeability. Others affect the aggregation of platelets, which is a part of the clotting process.

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The plasma accumulated at the site of injury contains interrelated enzyme systems such as, the complement system, kinins, coagulation factors, and the fibrinolytic system that generate various mediators of inflammation.

Activated complement proteins serve as chemotactic factors for neutrophils, increase vascular permeability, and stimulate the release of histamine from mast cells. They also adhere to the surface of bacteria, making them easier targets for phagocytes.

The kinin system, which is activated by coagulation factor XII, produces substances that increase vascular permeability. Bradykinin, the most important of the kinins, is responsible for much of the pain and itching experienced with inflammation.

The coagulation factors convert the plasma protein fibrinogen into fibrin, a major component of the fluid exudates. The fibrinolytic system contributes to inflammation primarily through the formation of plasmin, which breaks down fibrin into products that affect vascular permeability.

2. Vascular Changes:

The first vascular change is vasoconstriction. When a tissue is injured, the small blood vessels in the damaged area constrict momentarily.

Following this transient event, the blood vessels dilate (vasodilation), under the influence of regulatory molicules on endothelial cells of blood vessels. When blood vessels dilate the walls of the blood vessels become more permeable and allow protein-rich fluid (exudates) along with water and salts into the tissues of damaged area.

Substances in the exudates include clotting factors that help in preventing the spread of infectious agents throughout the body. Other proteins include antibodies that help in destroying invading microorganisms.

As fluid and other substances leak out of the blood vessels, blood flow becomes more sluggish and white blood cells begin to fall out of the axial stream in the centre of the vessel to flow nearer the vessel wall. Vasodilation may last from 15 minutes to several hours.

3. Cellular Changes:

Accumulation of white blood cells (phagocytic cells) at the site of injury is the most important feature of inflammation. The main phagocytes involved in acute inflammation are the neutrophils.

Within an hour after injury or infection large number of neutrophils reach the site of injury. When tissue damage is minor, an adequate supply of neutrophils can be obtained from those already circulating in the blood.

But, when damage is extensive, neutrophils from reservoirs move to perform their tasks. If the demand is high, even immature forms of neutrophils directly from the bone marrow also reach the site.

The movement of neutrophils from the blood vessel (diapedisis) towards the area of tissue damage is made possible by chemical substances that diffuse from the area of tissue damage and create a concentration gradient followed by the neutrophils.

In many cases subsequent to 24 to 28 hours of the inflammation another group of white blood cells, the monocytes, reach the site and mature into cell-eating macrophages.

Hence macrophages usually become more prevalent at the site of injury only after days or weeks of injury and are a cellular hallmark of chronic inflammation. If the inflammation is caused by parasitic worms, against which neutrophils have little success, eosinophils rather than neutrophils predominate in acute inflammation.

Eosinophils release several proteins that are often effective against parasites. Generally eosinophils are linked to certain types of allergies.

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