Probiotics improves sepsis-induced acute lung injury in association with intestinal microbiota and pulmonary concentrations of Th17 and Treg

Abstract

This study aims to assess the immune status of septic acute lung injury (ALI) at various stages and to investigate whether probiotics can mitigate ALI in septic rats. Rats were randomly assigned to sham, caecal ligation and puncture (CLP), and probiotic treatment after CLP (CLP+PT) group. Intestinal contents, bronchoalveolar lavage fluid (BALF), and lung tissue were collected from rats at 6, 24 and 48 h after CLP. Results showed that Th17 level at 24 h in BALF is significantly higher than that at 6 and 48 h. The Treg level increased after CLP and reached its highest point at 48 h. Pathological damage in the alveolar interstitium intensified over time. At 24 h, Th17 percentage of BALF significantly increased in the CLP group while it significantly decreased in the CLP+PT group, and the Treg percentage of BALF at 48 h showed the same alteration trend. Alveolar interstitial pathological damage in the CLP+PT group was reduced at all time points compared to the CLP group. The abundance of Firmicutes was higher and Bacteroidetes lower in the sepsis group compared to the sham group. However, the abundance of these bacteria was similar between the probiotic and pseudo-probiotic groups. Actinomycetes levels differed significantly among the three groups, with the probiotic group exhibiting significantly higher levels. Bifidobacteria levels were significantly higher in the probiotic group compared to the sepsis group. Phenotype prediction indicated a higher proportion of biofilm formation in the probiotic group compared to the sepsis group. In conclusions, significant alterations in Th17 and Treg levels in BALF of septic rats suggest a shift in the distribution of important T lymphocytes in the lungs during sepsis. Probiotics modulated the gut microbiota of septic rats, downregulated the highest value of Th17 and Treg percentage in BAFL, resulting in mitigated lung injury in rats.