Extended Data Fig. 8: Salmonella PflB does not affect host morbidity during foodborne infection. | Nature

Extended Data Fig. 8: Salmonella PflB does not affect host morbidity during foodborne infection.

From: Microbes exploit death-induced nutrient release by gut epithelial cells

Extended Data Fig. 8

a, Salmonella burden of WT (black) or ΔcadBA (CJA033, green). n = 7 mice from 2 cohorts. b, Salmonella burden of WT (black) or ΔpflB (CJA057, blue). n = 6 SPF mice from 2 cohorts. n = 9 germ-free mice from 2 cohorts. *P ≤ 0.05, **P ≤ 0.005 two-tailed Wilcoxon signed rank test with theoretical median of 1 using the calculated competitive index from each mouse. c, Body weight (mean ± s.e.m. is shown). n = 15 (WT), n = 10 ΔSPI-1ΔSPI-2, n = 8 ΔpflB mice from 4 cohorts. ns, P > 0.05. *P ≤ 0.05, ***P ≤ 0.0005, two-way ANOVA (body weight) or one-way ANOVA (caecal weight, colon length) with Tukey’s multiple comparisons test. d, Caecal weight. n = 15 (WT), n = 10 ΔSPI-1ΔSPI-2, n = 8 ΔpflB mice from 4 cohorts. ns, P > 0.05. *P ≤ 0.05, ***P ≤ 0.0005, one-way ANOVA with Tukey’s multiple comparisons test. e, Colon length n = 15 (WT), n = 10 ΔSPI-1ΔSPI-2, n = 8 ΔpflB mice from 4 cohorts. ns, P > 0.05. *P ≤ 0.05, ***P ≤ 0.0005, one-way ANOVA with Tukey’s multiple comparisons test. f, Salmonella burden of WT (black), ΔSPI-1ΔSPI-2 (CJA077, orange) or ΔpflB (CJA057, blue). n = 15 WT, n = 8 ΔSPI-1ΔSPI-2, n = 8 ΔpflB from 4 cohorts. ns, P > 0.05. **P ≤ 0.005, Kruskal–Wallis with Dunn’s multiple comparisons test. g, Competitive index either (black) WT Salmonella compared to ΔpflB (CJA057) or (orange) ΔSPI-1ΔSPI-2 (CJA077) compared to ΔSPI-1ΔSPI-2ΔpflB (CJA081). n = 14 mice from 4 cohorts. ns, P > 0.05. *P ≤ 0.05, two-tailed Mann–Whitney U-test. h, Cleaved caspase 3 staining in colons. Scale bars, 500 μm (top), 100 μm (zoomed in box). i, Percentage body weight of Casp3/7fl/fl control or Vil-cre+/−Casp3/7fl/fl mice after Salmonella infection (as in Fig. 3). n = 11 female Casp3/7fl/fl control mice, n = 7 female Vil-cre+/−Casp3/7fl/fl mice from 3 cohorts. Data are mean ± s.e.m. j, Caecal weight of Casp3/7fl/fl control or Vil-cre+/−Casp3/7fl/fl mice after Salmonella infection (as in Fig. 3). n = 8 female Casp3/7fl/fl control mice, n = 7 female Vil-cre+/−Casp3/7fl/fl mice from 2 cohorts. ns, P > 0.05, unpaired two-tailed Student’s t-test. k, Colon length of Casp3/7fl/fl control or Vil-cre+/−Casp3/7fl/fl mice after Salmonella infection (as in Fig. 3). n = 5 female Casp3/7fl/fl control mice, n = 5 female Vil-cre+/−Casp3/7fl/fl mice from 2 cohorts. ns, P > 0.05, unpaired two-tailed Student’s t-test. l, Salmonella burden in the indicated tissue of Casp3/7fl/fl control or Vil-cre+/−Casp3/7fl/fl mice at day 4 after infection. n = 11 female Casp3/7fl/fl control mice, n = 7 female Vil-cre+/− Casp3/7fl/fl mice from 3 cohorts. m, Competitive index of wild-type Salmonella compared to ΔpflB (CJA057) in the indicated tissue of Casp3/7fl/fl control or Vil-cre+/−Casp3/7fl/fl mice at day 4 after infection. n = 8 female Casp3/7fl/fl control mice, n = 5 female Vil-cre+/−Casp3/7fl/fl mice from 2 cohorts. ns, P > 0.05. *P ≤ 0.05, two-tailed Mann–Whitney U-test with each tissue analysed separately. Box plots are as in Fig. 1. In a and b, wild-type and mutant Salmonella connected with dotted lines come from the same mouse. The median competitive index is listed below each tissue. ns, P > 0.05. *P ≤ 0.05, two-tailed Wilcoxon signed rank test with theoretical median of 1 using the calculated competitive index from each mouse

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