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. Author manuscript; available in PMC: 2019 May 1.
Published in final edited form as: J Immunol. 2018 Mar 21;200(9):3188–3200. doi: 10.4049/jimmunol.1700834

Fig. 7.

Fig. 7

Whole-brain S100A8 expression after sepsis is reduced by TNFα deficiency (A). S100A9 deficiency abolishes priming of microglial TNFα production after CLP. Fourteen days after CLP, microglia express modestly elevated levels of TNFα mRNA (B, t test p=0.009). When cultured ex vivo, microglia isolated from sepsis survivor mice do not secrete increased amounts of TNFα (C). After stimulation with LPS, however, microglia isolated from sepsis survivor mice 14 days after CLP exhibit marked potentiation of TNFα secretion (C). Microglia isolated from S100A9−/− mice 5 days after CLP do not exhibit potentiation of LPS-stimulated TNFα secretion, compared to wild-type sepsis survivors (C, 2-way ANOVA, p<0.0001 for effect of genotype). * p < 0.05, ** p < 0.01