Integrin alpha E beta 7 is involved in the intestinal barrier injury of sepsis

Background: IL-9-producing CD4(+) T (Th9) cell was related to acute intestinal barrier injury in sepsis. Integrin alpha E beta 7 was an important lymphocyte homing receptor on the surface of intestinal Th9 cells. However, the roles of alpha E beta 7 in the intestinal injury caused by Th9 cells were not clear in sepsis. Methods: To investigate the roles of alpha E beta 7 in the intestinal injury caused by Th9 cells in sepsis model, the Th9 cells percentages, alpha E beta 7 , E-cadherin, IL-9, and D-lactate levels in both serum and intestinal tissue were measured. The intestinal histopathology, epithelium apoptosis, and mucosal permeability measurement were also performed. The survival rate of septic rats was recorded daily for 14 days. Results: Rats were assigned to four cohorts: control cohort, sepsis cohort, sepsis+alpha E beta 7i (alpha E beta 7 inhibition) cohort, and sepsis+alpha E beta 7e (alpha E beta 7 overexpression) cohort. The Th9 cells percentages, alpha E beta 7, IL-9, and D-lactate levels of the sepsis cohort were significantly higher than those of the control cohort. The levels of these variables were also elevated progressively in the sepsis+alpha E beta 7i cohort, sepsis cohort, and sepsis+alpha E beta 7e cohort. The E-cadherin levels were decreased progressively in the control cohort, sepsis+alpha E beta 7i cohort, sepsis cohort, and sepsis+alpha E beta 7e cohort. Moreover, alpha E beta 7 overexpression could decrease the 14-day survival rate. The findings of histopathology staining, apoptosis detection, and intestinal permeability test also confirmed that the barrier injury was deteriorated or relieved by elevating or decreasing the alpha E beta 7 expression levels, respectively. Conclusions: Integrin alpha E beta 7 was closely associated with the intestinal barrier injury caused by Th9 lymphocytes in sepsis.