Анализ воспалительного процесса в параметрах функции нейтрофилов

Из-за различных причин патогенный раздражитель не подвергается уничтожению либо возникает потом в механизмах самой воспалительной реакции (апоптоз фагоцитирующих клеток) В этом случае воспаление приобретает хроническое течение. По существу, персистенция воспалительных проявлений является элементом возникшего дефекта в системе защиты и приспособления организма к меняющимся условиям существования. Вопросы патогенеза, механизмы прогрессирования и хронизации патологического процесса во многом обусловлены нарушенными параметрами апоптоза нейтрофилов.

Analysis of inflammatory process in parameters of function of neutrophils

Binding of immune complexes to cell receptors for immunoglobulin is a powerful stimulus to activation of phagocytes. Immune complex binding to these cells leads to activation of effector functions of host defense such as phagocytosis, secretion, cytokine synthesis, and the production of toxic oxygen metabolites, which occurs as a result of NADPH oxidase assembly. Immune complexes are potent stimuli for activation of PMN. Immune complex deposition and subsequent PMN activation is an important part of the pathogenesis of serum sickness, the Arthus reaction, acute glomerulonephritis, rheumatoid arthritis, and other idiopathic inflammatory diseases. Although these are host-damaging diseases, immune complex-mediated PMN activation also plays an essential role in host defense against bacterial infection. It is clear that in vivo both host defense and host damaging aspects of the PMN-immune complex interaction involve complement activation and deposition onto the immune complexes. Activated PMNs are removed from tissue by apoptosis, but inflammatory mediators such as lipopolysaccharide (LPS) can delay PMN apoptosis thereby prolonging inflammation. Polymorphonuclear leukocytes (PMN) play a primary role in the initiation and propagation of inflammatory responses. PMN apoptosis is a major mechanism associated with the resolution of inflammatory reactions. Understanding mechanisms associated with PMN apoptosis will be of critical value in the development of novel pharmacological treatment strategies for local and/or systemic inflammatory disorders. The present study demonstrates that immune complex no induces human PMN to undergo rapid and synchronous progression into the apoptotic process via a PKC-independent mechanism.