Translocation and Dissemination of Gut Bacteria after Severe Traumatic Brain Injury

Abstract

Enterobacteriaceae are often found in the lungs of patients with severe Traumatic Brain Injury (sTBI). However, it is unknown whether these bacteria come from the gut microbiota. To investigate this hypothesis, the mice model of sTBI was used in this study. After sTBI, Chao1 and Simpson index peaking at 7 d in the lungs (p < 0.05). The relative abundance of Acinetobacter in the lungs increased to 16.26% at 7 d after sTBI. The chao1 index of gut microbiota increased after sTBI and peaked at 7 d (p < 0.05). Three hours after sTBI, the conditional pathogens such as Lachnoclostridium, Acinetobacter, Bacteroides and Streptococcus grew significantly. At 7 d and 14 d, the histology scores in the sTBI group were significantly higher than the control group (p < 0.05). The myeloperoxidase (MPO) activity increased at all-time points after sTBI and peaked at 7 d (p < 0.05). The LBP and sCD14 peaking 7 d after sTBI (p < 0.05). The Zonulin increased significantly at 3 d after sTBI and maintained the high level (p < 0.05). SourceTracker identified that the lung tissue microbiota reflects 49.69% gut source at 7 d after sTBI. In the small intestine, sTBI induced gastrointestinal dysfunction with increased apoptosis and decreasing antimicrobial peptides. There was a negative correlation between gut conditional pathogens and the expression level of antimicrobial peptides in Paneth cells. Our data indicate that gut bacteria translocated to the lungs after sTBI, and Paneth cells may regulate gut microbiota stability and translocation.