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. Author manuscript; available in PMC: 2020 Mar 18.
Published in final edited form as: Nature. 2019 Sep 18;574(7776):57–62. doi: 10.1038/s41586-019-1570-z

Figure 4 |. Contribution of mouse N-formylpeptide receptors to plague disease.

Figure 4 |

a, Transfection with pmFpr1, but not pmFpr2 or pmFpr3, restores Y. pestis KIM D27 (pMM83) translocation of YopM-Bla into U937 FPR1−/− cells. One of three repeats is shown and error bars represent the s.e.m. (n = 3 biological replicates). b, Compared to C57BL/6 mice, BMDM from mFpr1−/−, but not mFpr2−/− mice, exhibit increased survival when infected with Y. pestis POO1 (yopE-dtx); one of three repeats is shown and error bars represent the s.e.m (n = 3 biological replicates). Y. pestis KIM D27 (pMM83) translocation of YopM-Bla in mouse BMDM (c) and neutrophils (d) requires mFpr1; one of three repeats is shown and error bars represent the s.e.m. (n = 3 biological replicates). e, Survival of wild-type C57BL/6 and mFpr1−/− mice (n=10 males and 10 females) following subcutaneous inoculation with (600 CFU) Y. pestis CO92. f, Bacterial loads (CFU) in spleen tissues of dead and surviving animals. Horizontal bars denote the mean and error bars represent the s.e.m. One of two repeats is shown (e, f). Significant differences were determined using one-way ANOVA and Bonferroni’s post-hoc analysis (a-d) and the log-rank (Mantel-Cox) test (e): ***, P<0.001.