Stress-induced local inflammation correlates with an increase in inflammatory myeloid cells

Abstract

The correlation between chronic stress and aggravation of inflammatory diseases has long been implied. A variety of studies in men and mice have proven the increase in myeloid cell blood counts as a hallmark of stressor exposure. Redistribution of myeloid cells from primary and secondary lymphoid organs into the blood is thought to be the major reason for that phenomenon. Recently, we established a model of chronic subordinate colony housing (CSC) in male mice. CSC induced an aggravation of DSS-induced colitis. Gut inflammation was accompanied with an increased translocation of commensal bacteria from the gut lumen into the surrounding tissue. We now analysed changes in the composition and function of myeloid cell subtypes in spleen and gut. CSC stress induced an increase in myeloid cells in blood, spleen and gut. A detailed analysis revealed that CD11b + cells in the spleen consisted mainly of Ly6G + granulocytic cells. Furthermore, myeloid cells from the spleen reacted with an increased cytokine production to in vitro restimulation with LPS indicating an inflammatory phenotype of those cells. CSC also induced up-regulation of CXCL1 and CXCL2 in the spleen and in the gut. Our study showed a stress-induced accumulation of distinct myeloid cells in secondary lymphoid organs and peripheral tissue that seemed to be mediated by specific chemokines induced during exposure to CSC. Due to their inflammatory phenotype these cells might contribute to the aggravation of local gut inflammation seen in the DSS-induced colitis.