Abstract

The trigger in the violation of the immune response in sepsis is the release of a large number of pro- and antiinflammatory mediators, primarily cytokines and other biologically active substances. Despite the fact that a sufficient number of studies have been carried out in which an increase in the amount of cytokines in sepsis has been noted, there is no work on the study of similar changes in the skin, which is the largest protective barrier in the body, and, accordingly, plays a significant role in maintaining the immune homeostasis. The aim of the study was to assess the expression of pro- and anti-inflammatory skin mediators in experimental sepsis. Materials and Methods. Mice were used as experimental animals, which underwent surgery CLP. The object of the study is the skin, which was studied using the immunohistochemical method (antibodies to TGF-a, TGF-a, IL-12, IL-10, IL-6, CD206, CD163, CD68). Results. In case of sepsis, an increase in the proportion of immunopositive cells in the epidermis and dermis was found: TNF-(33.1 ± 1.2%); TGF-a (35.3 ± 1.4%); IL-12 (6.8 ± 0.3%); IL-10 (9.2 ± 0.9%); IL-6 (28.2 ± 0.8%); CD206 (12.9 ± 0.7%); CD163 (16.1 ± 0.8%); CD68 (28.4 ± 0.9%). Conclusion. An increase in the number of pro-inflammatory and anti-inflammatory cytokines in sepsis indicates the involvement of the epidermis in the general inflammatory process, due to a shift in the cytokine balance towards the predominance of pro-inflammatory mediators and M1-macrophages

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