Abstract
Background: IL-9-producing CD4(+) T (Th9) cell was related to acute intestinal barrier injury in sepsis. Integrin αEβ7 was an important lymphocyte homing receptor on the surface of intestinal Th9 cells. However, the roles of αEβ7 in the intestinal injury caused by Th9 cells were not clear in sepsis.Methods: To investigate the roles of αEβ7 in the intestinal injury caused by Th9 cells in sepsis model, the Th9 cells percentages, αEβ7, 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+αEβ7i (αEβ7 inhibition) cohort, and sepsis+αEβ7e (αEβ7 overexpression) cohort. The Th9 cells percentages, αEβ7, 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+αEβ7i cohort, sepsis cohort, and sepsis+αEβ7e cohort. The E-cadherin levels were decreased progressively in the control cohort, sepsis+αEβ7i cohort, sepsis cohort, and sepsis+αEβ7e cohort. Moreover, αEβ7 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 αEβ7 expression levels, respectively.Conclusions: Integrin αEβ7 was closely associated with the intestinal barrier injury caused by Th9 lymphocytes in sepsis.
Highlights
Sepsis is a potentially fatal disease characterized by organ dysfunction as a result of an improperly controlled host response to pathogens [1, 2]
The serum Th9 cells proportions of the sepsis+αEβ7e cohort were shown to be elevated in contrast with those of the sepsis cohort (2.98% ± 0.64% vs. 1.63% ± 0.46%, P
The serum Th9 cell proportions of the sepsis cohort were elevated in contrast with those of the sepsis+αEβ7i cohort (1.63% ± 0.46% vs. 0.93% ± 0.26%, P =0.027)
Summary
Sepsis is a potentially fatal disease characterized by organ dysfunction as a result of an improperly controlled host response to pathogens [1, 2]. Methods: To investigate the roles of αEβ7 in the intestinal injury caused by Th9 cells in sepsis model, the Th9 cells percentages, αEβ7, E-cadherin, IL-9, and D-lactate levels in both serum and intestinal tissue were measured. The Th9 cells percentages, αEβ7, 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 elevated progressively in the sepsis+αEβ7i cohort, sepsis cohort, and sepsis+αEβ7e cohort. The findings of histopathology staining, apoptosis detection, and intestinal permeability test confirmed that the barrier injury was deteriorated or relieved by elevating or decreasing the αEβ7 expression levels, respectively. Conclusions: Integrin αEβ7 was closely associated with the intestinal barrier injury caused by Th9 lymphocytes in sepsis
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