AUTOINFLAMMATORY DISEASES IN HEMATOLOGY FROM DIAGNOSIS TO TREATMENT

AUTOINFLAMMATORY_DISEASES_IN_HEMATOLOGY_FROM_DIAGNOSIS_TO_TREATMENTkapak

PHYSIOLOGY OF INFLAMMATION

Aslı Kum

Aksaray Training and Research Hospital, Department of Hematology, Aksaray, Türkiye

Kum A. Physiology of Inflammation. In: Kurt Yüksel M, editor. Autoinflammatory Diseases in Hematology from Diagnosis to Treatment. 1st ed. Ankara: Türkiye Klinikleri; 2025. p.3-14.

ABSTRACT

Exogenous and endogenous stimuli that cause cell injury can lead to a complex reaction called inflammation in vascularized connective tissues. Briefly, inflammation is a protective response that aims to destroy the factor that causes cell damage and to eliminate the necrotic tissue and cells result from the destruction. It accomplishes this protective function by diluting, breaking down, and otherwise neutralizing harmful agents (such as microbes or toxins). It initiates a series of events that will repair the damaged tissue and ultimately allow healing. Therefore, inflammation may be characterized by the renewal of damaged tissue by regeneration of parenchymal cells or by filling of the remaining defect with fibrous scar tissue. Inflammation helps to destroy infection and repair heal injury, otherhand both processes have the potential to cause significant damage. There are many factors in the inflammatory response, including circulating cells,plasma proteins, vascular wall cells, extracellular matrix and cells of the surrounding connective tissue. Circulating cells are polymorphonuclear leukocytes (neutrophils), eosinophils, basophils, lymphocytes, monocytes, and platelets produced by bone marrow. Circulating proteins such as coagulation factors, kininogens, and complement components synthesized by the liver. The vascular wall cells are the endothelial cells that are in direct contact with the blood. The smooth muscle cells lie beneath the vessels and provide tone to the vessels. Connective tissue cells are consist of mast cells, macrophages, and lymphocytes, which guard against invasion, as well as fibroblasts synthesize extracellular matrix and can proliferate to fill the wound. The extracellular matrix (ECM) consists of fibrous proteins (such as collagen and elastin), which are cell-ECM and ECM-ECM connectors, gel-forming proteoglycans, and adhesion glycoproteins (such as fibronectin).

Inflammation is defined by two categories: acute and chronic form. Acute inflammation is a sudden and early response to injury that occurs when leukocytes reach the injury site. The course of events in acute inflammation is regulated by locally released chemical mediators. Vascular changes and cellular aggregation cause three of the five classic local findings of acute inflammation: heat (calor), redness (rubor), and swelling (tumor). The other two main features of acute inflammation are pain (dolor) and loss of function (functio laesa). These result from mediator release and leukocyte-mediated injury. Although the termination of acute inflammation varies depending on some factors such as severity of inflammation, nature and location of the injury, the tissue type and also the host’s ability to respond, The consequences of acute inflammation generally end in one of three possibilities. These are; resolution, scarring or fibrosis with progression to chronic inflammation. Chronic inflammation has a cellular infiltrate consisting of monocytes, macrophages, and lymphocytes. It has slow onset with prolonged duration. Additionally it has less pronounced classic signs and symptoms. Chronic inflammation may result from persistent infections of microorganisms which are difficult to be eradicated such as mycobacteria, viruses, fungi, and parasites. It may trigger delayed-type hypersensitivity reactions which may lead to granulomatous responses or unresolved acute inflammation that evolves into a chronic condition.

Keywords: Inflammation; Cytokines; Fibrosis

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