TRIM32-TAX1BP1-dependent selective autophagic degradation of TRIF negatively regulates TLR3/4-mediated innate immune responses
Fig 3
TRIM32-deficiency potentiates Salmonella typhimurium-induced immune responses in vivo.
(A) Effects of TRIM32-deficiency on clearance of Salmonella typhimurium in vivo. Sex- and age-matched Trim32+/+ and Trim32-/- mice were orally infected with Salmonella typhimurium, and bacterial loads were assessed in the indicated tissues 8 days post infection. (B) Effects of TRIM32-deficiency on Salmonella typhimurium-induced lymphocyte activation. Sex- and age-matched Trim32+/+ and Trim32-/- mice were orally infected with Salmonella typhimurium, and viable cell numbers of spleen were counted 6 days post infection. (C) Effects of TRIM32-deficiency on Salmonella typhimurium-induced secretion of inflammatory cytokines. Sex- and age-matched Trim32+/+ and Trim32-/- mice (n = 3) were orally infected with Salmonella typhimurium for 6 days, followed by measurement of the levels of inflammatory cytokines in the sera. (D) Effects of TRIM32-deficiency on Salmonella typhimurium-induced inflammatory damage of the intestines of mice. Sex- and age-matched Trim32+/+ and Trim32-/- mice were orally infected with Salmonella typhimurium, and the intestines of mice were used for histological analysis (H&E staining). (E) Effects of TRIM32-deficiency on Salmonella typhimurium-induced loss of body weight. Sex- and age-matched Trim32+/+ (n = 11) and Trim32−/− (n = 7) mice were orally infected with Salmonella typhimurium, and their body weight were monitored every day for 7 days. (F) Effects of TRIM32-deficiency on Salmonella typhimurium-induced inflammatory death. Sex- and Trim32+/+ (n = 6) and Trim32-/- mice (n = 7) were infected with Salmonella typhimurium, and the survival rates of the mice were monitored every day for 20 days. *, p<0.05; **, p<0.01.