Figure 1.

Characterization of severe SAE and light SAE mice and dependence of sepsis-induced brain injury on gut microbiota. Survival rates of mice were observed until 7 days post-CLP. Mice that died within 48 hours of CLP were defined as severe SAE (SSAE) because of the high mortality. Mice that survived after 7 days were defined as light SAE (LSAE) because of the mortality rate tends to be flat. (A) Survival rate. (B) Neurobehavioral scores. (C) Representative H&E-stained sections of hippocampus of SSAE and LSAE mice. (D) Western blot analysis of iNOS, COX-2, and BDNF protein expressions in the hippocampus of SSAE and LSAE mice. GAPDH served as the loading control. Bar graphs depict the optical density of iNOS, COX-2, and BDNF expression. (E) Schematic illustration of FMT experiment: Mice were administered intragastric vancomycin (100 mg/kg), neomycin sulfate (200 mg/kg), metronidazole (200 mg/kg), and ampicillin (200 mg/kg) once-daily for 5 days to deplete the gut microbiota; subsequently, they received feces resuspended in PBS from SSAE and LSAE mice for 3 days. CLP surgery was performed, and mice were sacrificed 12 hours after CLP. (F) Representative H&E-stained sections of hippocampus of recipient mice. (G) Western blot analysis of iNOS, COX-2, and BDNF protein expressions in the hippocampus of recipient mice. GAPDH served as the loading control. Bar graphs depict the optical density of iNOS, COX-2, and BDNF expressions. Data presented as mean ± SD (n = 3–8 per group). Scale bars: 100µm and 20µm. *P < 0.05, **P < 0.01, ***P < 0.001 by Student’ t-test.