Копия Inflammation and Repair. Mediators of inflamation-2020.pptx

Pathology

1. Inflammation and Repair

2. The survival of all organisms requires that they eliminate foreign invaders, such as infectious agents, and damaged tissues. These functions are mediated by a complex host response called inflammation. Inflammation is a protective response involving host cells, blood vessels, and proteins and other mediators that is intended to eliminate the initial cause of cell injury, as well as the necrotic cells and tissues resulting from the original insult, and to initiate the process of repair. Inflam - mation accomplishes its protective mission by first diluting, destroying, or otherwise neutralizing harmful agents (e.g., microbes, toxins). It then sets into motion the events that eventually heal and repair the sites of injury. Without inflammation, infections would go unchecked and wounds would never heal. In the context of infections, inflammation is one component of a protective response that immunologists refer to as innate immunity The cells and molecules of host defense, including leukocytes and plasma proteins, normally circulate in the blood, and the goal of the inflammatory reaction is to bring them to the site of infection or tissue damage. In addition, resident cells of vascular walls and the cells and proteins of the extracelular matrix (ECM) are also involved in inflammation and repair

3. Inflammation can be acute or chronic Acute inflammation is rapid in onset and of short duration, lasting from a few minutes to as long as a few days, and is characterized by fluid and plasma protein exudation and a predominantly neutrophilic leukocyte accumulation. Chronic inflammation may be more insidious, is of longer duration (days to years), and is typified by influx of lymphocytes and macrophages with associated vascular pro- liferation and fibrosis (scarring). Inflammation is induced by chemical mediators that are produced by host cells in response to injurious stimuli. When a microbe enters a tissue or the tissue is injured, the presence of the infection or damage is sensed by resident cells, mainly macrophages, but also dendritic cells, mast cells, and other cell types.

4. These cells secrete molecules (cytokines and other mediators) that induce and regulate the subsequent inflammatory response. Inflammatory mediators are also produced from plasma proteins that react with the microbes or to injured tissues. Some of these mediators promote the efflux of plasma and the recruit- ment of circulating leukocytes to the site where the offending agent is located. The recruited leukocytes are activated and they try to remove the offending agent by phagocytosis. An unfortunate side effect of the activation of leukocytes may be damage to normal host tissues.

5. The external manifestations of inflammation, often called its cardinal signs, are heat ( calor ), redness ( rubor ), swelling (tumor), pain (dolor), and loss of function ( functio laesa ). The first four of these were described more than 2000 years ago by a Roman encyclopedist named Celsus , and the fifth was added in the late 19th century by Rudolf Virchow, known as the “father of modern pathology.” These manifestations occur as consequences of the vascular changes and leukocyte recruitment and activation. Inflammation is normally controlled and self-limited. The mediators and cells are activated only in response to the injurious stimulus and are short-lived, and they are degraded or become inactive as the injurious agent is eliminated. In addition, various anti-inflammatory mechanisms become active. If the injurious agent cannot be quickly eliminated, the result may be chronic inflammation, which can have serious pathologic consequences .

6. Summary. General Features of Inflammation Inflammation is a defensive host response to foreign invaders and necrotic tissue, but it is itself capable of causing tissue damage. The main components of inflammation are a vascular reaction and a cellular response; both are activated by mediators derived from plasma proteins and various cells. The steps of the inflammatory response can be remembered as the five Rs : (1) recognition of the injurious agent, (2) recruitment of leukocytes, (3) removal of the agent, (4) regulation (control) of the response, and (5) resolution (repair). The outcome of acute inflammation is either elimination of the noxious stimulus, followed by decline of the reac - tion and repair of the damaged tissue, or persistent injury resulting in chronic inflammation.

7. Histamines attach to the cells in our body . They cause the cells to swell and leak fluid. This can cause itching, sneezing, runny nose, and watery eyes. Antihistamines prevent histamines from attaching to your cells and causing symptoms Kininogens are precursor proteins for kinins , biologically active polypeptides involved in blood coagulation, vasodilation, smooth muscle contraction, inflammatory regulation, and the regulation of the cardiovascular and renal systems The two main types are: ⁕High-molecular-weight kininogen , which is produced by the liver together with prekallikrein . It acts mainly as a cofactor on coagulation and inflammation, and has no intrinsic catalytic activity. These high molecular weight kininogens are cleaved into bradykinin and kallidin by tissue and plasma kallikreins . ⁕Low-molecular-weight kininogen , which is produced locally by numerous tissues, and secreted together with tissue kallikrein . They are both spliced from the same precursor.