Regularities and direction of change in the gut immune system in conditions of chronic social stress

Abstract

Investigated the influence of chronic social stress (CSS) on the distribution of TLR2+/4+, NF-kB+ -, T-bet+ -, GATA3+ -, Rorγt+ -, Foxp3+ -, LMP2+ -, XBP1+ - lymphocytes in the gut-associated lymphoid tissue. The purpose. Identify the features of the distribution of TLR2+/4+, NF-kB+-, T-bet+ -, GATA3+ -, Rorγt+ -, Foxp3+ -, LMP2+ -, XBP1+ lymphocytes in the gut-associated lymphoid tissue of rats with CSS. Methods. Researchеs have been conducted on 60 rats (female) of Wistar line, which were divided on 3 experimental groups: control rats (group 1); rats, which were modeled CSS1 by means of three weeks social isolation and prolong psychoemotional influence (group2); rats, which having CSS 2 modeling by means of keeping animals in over populated cages with every day change of grouping (group 3). Structure of population of TLR2+-, TLR4+-, Nf-kB+,- T-bet+-, GATA3+-, Rorγt+ -, Foxp3+ -, LMP2+ - and XBP1+ - cells has been studied by the analysis of serial histological sections using the method of direct and indirect immunofluorescense with monoclonal antibodies to TLR2, TLR4, Nf-kB, T-bet, GATA3, Rorγt, Foxp3, LMP2 and XBP1. Results. It has been established that the CSS development leads to a significant activation of the innate immune system and accompanied by an imbalance of T-helper subsets in GALT, leads to an increase in ratio of T-bet+/GATA3+ and reduce Foxp3+/Rorγt+- cells, indicating dominance Th1- and Th17-differentiation in conditions of CSS and raising the level of pro-inflammatory signaling in the gut. In addition, it has been shown that on the background of chronic social stress develops immunoproteasomny defect and endoplasmic reticulum stress, which is accompanied by a unidirectional trend to increase the total number of LMP2+ lymphocytes and reduce the total number of XBP1+cells, and the concentration change LMP2 and XBP1 immune cells depends on the type of stress. Conclusion. The results showed that chronic social stress may be one of the triggers for development of inflammatory and AID.