Инфекция и иммунитет (Sep 2018)
DISTURBANCE OF AN APOPTOSIS OF NEUTROPHILS AT A SEPSIS
Abstract
The sepsis represents life-endangering disturbances of functions of the internals caused by a dizregulyation of a macroorganism to the infectious agent and is difficult interaction of pro-inflammatory and antiinflammatory processes that not seldom defines the fate of patients. The predetermining factor of a sepsis is the originator. The immunosupression caused by the originator promotes generalization of an infection, and the intensive bacteriemia caused by generalization leads to the accruing endotoxinemia that aggravates immunosupression even more and leads finally to systemic inflammatory reaction — the main and most dangerous implication of a sepsis. The syndrome of systemic inflammation with uncontrollable emission of cytokines is the cornerstone of a sepsis. The pathophysiology of a sepsis begins with impassioned inflammatory reaction which can last several days, and then passes into more lingering immunosupressivny period where the outcome depends on the immune system of the patient. Cellular apoptosis is one of leaders in sepsis immunosupression development. In article mechanisms of disturbance of an apoptosis of neutrophils are described that, undoubtedly, affects weighting of a current of a sepsis and as a result, a failure. Migration of neutrophils under natural conditions includes four various phases which during a sepsis are broken. The mechanisms worsening migration of neutrophils, contributing to the development of a sepsis were investigated in numerous scientific works. Authors of Peking University offered schemes of a way of disturbance of an apoptosis of neutrophils and migration of neutrophils at a sepsis. Despite the extensive accumulated experience on studying of a pathogenesis of septic states, there are no effective and specific remedies of fight from a sepsis now. Perhaps, by prevention of disturbance of the programmed death of a cell the cytokines developed anti-apoptotic, caspase inhibitors will be.
Keywords