Acute Inflammation
المؤلف:
Mary Louise Turgeon
المصدر:
Immunology & Serology in Laboratory Medicine
الجزء والصفحة:
5th E, P38-39
2025-06-10
615
Tissue damage results in inflammation, a series of biochemical and cellular changes that facilitate the phagocytosis of invading microorganisms or damaged cells (Fig.1). If inflammation is sufficiently extensive, it is accompanied by an increase in the plasma concentration of acute-phase reactants. Leukocyte recruitment into inflamed tissue follows a well-defined cascade of events beginning with the capture of free-flowing WBCs to the vessel wall and subsequent leukocyte rolling along and adhesion to the inflamed endothelial layer. During rolling, WBCs come into close contact with the endothelial surface, which allows endothelium-bound chemokines to interact with their specific receptors on the leukocyte sur face. This triggers the activation of integrins, which leads to firm leukocyte arrest on the endothelium. In addition, integrin-dependent signaling events induce cytoskeletal rearrangements and cell polarization, modifications necessary to help prepare the attached leukocyte to spread and crawl in search for a way out of the vasculature into tissue.
Fig1. Acute inflammatory response. Neutrophils are among the first cells to arrive at the scene of an infection and are important contributors to the acute inflammatory response. As the neutrophil rolls along the blood vessel wall, the L-selectin on its surface binds to carbohydrate structures such as sialyl-Lewis X on the adhesion molecules on the vascular endothelium, and its progress is eventually halted. As the neutrophil becomes activated, it replaces L-selectin with other cell surface adhesion molecules, such as integrins. These molecules bind E-selectin, which is present on the blood vessel wall as a result of the influence of inflammatory mediators such as bacterial lipopolysaccharides and the cytokines IL-1 and TNF-α. The activated neutrophil then enters the tissues, where it is attracted to the infection site by a number of chemoattractants. The neutrophil can then phagocytose and destroy the C3b-coated bacteria. (Adapted from Delves PJ, Roitt IM: The immune system. First of two parts, N Engl J Med 343:37–49, 2000.)
Celsus, a practitioner of Greek medicine who was born in 25 BCE, is credited with recording the cardinal signs of inflammation—rubor (redness), calor (heat), dolor (pain), and tumor (swelling). The primary objective of inflammation is to localize and eradicate the irritant and repair the surrounding tissue. The inflammatory response involves the following three major stages:
1. Dilation of capillaries to increase blood flow
2. Microvascular structural changes and escape of plasma proteins from the bloodstream
3. Leukocyte transmigration through endothelium and accumulation at the site of injury
Hypoxia can induce inflammation. Inflammation in response to hypoxia is clinically relevant. Ischemia in organ grafts increases the risk of inflammation and graft failure or rejection. Hypoxia has multiple effects on the innate and adaptive immune systems.
Once inflammation is triggered, it must be appropriately resolved or pathologic tissue damage will occur. In some dis eases, the body’s defense system (immune system) inappropriately triggers an inflammatory response when no foreign substances are present. In these autoimmune disorders, the body’s normally protective immune system causes damage to its own tissues.
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