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. Author manuscript; available in PMC: 2016 May 1.
Published in final edited form as: Nat Immunol. 2015 Sep 28;16(11):1142–1152. doi: 10.1038/ni.3268

Figure 1. Losses of Mst1 and Mst2 increase susceptibility to bacterial sepsis.

Figure 1

(a) Representative lung tissues and H&E staining of lung sections from wild type and Mst1−/−Mst2fl/flVav-Cre mice. Scale bar, 100 μm.

(b-e) Mst1fl/flMst2fl/fl (WT) or Mst1fl/flMst2fl/flLyz2-Cre (cDKO) mice (n=10 mice per group per experiment) subjected to sublethal CLP; mortality (Mantel–Cox test)(b), serum cytokines measured by ELISAs (c), inflammatory cell infiltration in the lungs as shown by H&E staining (d) and the bacterial loads (colony forming units, CFU) measured in the lung, liver, spleen, kidney and peritoneal fluid (e) after CLP induction. Scale bar, 50 μm.

(f) Immunoblot analysis of P-p38, P-Jnk, IκBα and P-Mob1 in WT BMDMs stimulated with indicated TLR agonists for different durations.

(g) Immunoblot analysis of P-Mob1 and MyD88 in WT or MyD88 KO RAW246.7 cells stimulated with the indicated agonists for different durations.

(h) WT or cDKO BMDMs were stimulated with LPS for the indicated times, followed by immunoblot analysis with the indicated antibodies.

(i) WT and cDKO BMDMs or neutrophils were treated with LPS (100 ng/ml) for the indicated times. Cytokine (IL-6 and TNF) production was measured by ELISA.

Data were assessed with Student's t-test and are presented as mean ± s.d. ns, no significant, * p<0.05, ** p<0.01, *** p<0.001 compared with respective controls of biological replicates in c (n=3), e (n=5) and i (n=3). Data are one experiment representative of two (e) or three (a-d, f-i) independent experiments with similar results.