[Molecular and cellular mechanisms in inflammatory reactions]

Inflammation is a complex stereotypical reaction of the body expressing the response to damage of its cells and/or vascularized tissues. It is the body's reaction to invasion by an infectious agent, antigen challenge or even just physical, chemical, or traumatic damage. The development of inflammatory reactions is controlled by a number of cellular and molecular components. Leukocytes (namely neutrophils and macrophages) belong to the key inflammatory cells. Their accumulation in inflamed tissue results from adhesive interactions between leukocytes and endothelial cells within the microcirculation. The nature and magnitude of the adhesive interactions that take place within postcapillary venules are determined by a variety of factors, of which the contribution of different adhesion molecules (selectins, integrins, members of immunoglobulin superfamily) to leukocyte rolling, adherence, and emigration in venules is discussed. The main purpose of inflammation seems to be to bring fluids, proteins and cells from the blood into the damaged tissues for the elimination of injuring agent and triggering the healing and repairing processes. This is under the control of inflammation mediators which include vasoactive substances, proinflammatory and antiinflammatory cytokines, chemokines, acute phase reactants, bioactive lipids (prostanoids, platelet activating factor--PAF) and products of the plasma enzyme systems (complement, the coagulation clothing, kinin and fibrinolytic pathways) which are shortly reviewed. Several neuroendocrine hormones, neuropeptides, neurotransmitters and mainly glucocorticoids also play an important role of endogenous regulators of any inflammatory process. (Tab. 4, Fig. 1, Ref. 52.).