ANTI-INFLAMMATORY RESPONSE: NEUROENDOCRINE-IMMUNE INTERACTIONS

The role of inflammatory and anti-inflammatory responses in the course and outcome of crush syndrome, acute pancreatitis, and sepsis were analyzed. Clinical and experimental findings demonstrate that the level of inflammatory cytokines cannot be considered as a criterion for the degree of crush syndrome severity. Modeling of the crush syndrome in rats showed that despite the similar increase of inflammatory cytokines (IL-1 beta, TNF-alpha) in groups of different crush time, the level of increased anti-inflammatory cytokine IL-10 differed and correlated with the crush time. Moreover, it was also revealed that there is a significant relation (according to chi(2) criterion) between the lethality and absence of IL-10 levels decrease during the observed period. In patients with acute pancreatitis the IL-10 level was elevated and considered a criterion of severity degree. In addition, the dynamics of IL-10 level alteration is a marker for the course and outcome of a pathological process. The research presents an analysis on features of IL-10, the leading anti-inflammatory cytokine, which allows explaining why and in what conditions the high level of anti-inflammatory cytokine IL-10 may correlate with the severity degree, define the course and outcome of the illnesses, at which systemic inflammatory response is developed. The neuroendocrine-immune interactions play an important role in development of the anti-inflammatory response. It has been shown that the crush syndrome and acute pancreatitis destruct neuroendocrine-immune interactions. Furthermore, at acute pancreatitis there is a certain significant relation between the IL-10 level and derangement of neuroendocrine-immune interactions.