CXCL1 is controlled by MyD88 in lung epithelial cells and prolongs survival in MyD88^(−/−) mice following <i>A. fumigatus</i> challenge.

<p>(A) BALF (B) lung neutrophil recruitment in WT → WT (black bars), MyD88^(−/−) → WT (dark grey bars), WT → MyD88^(−/−) (light grey bars), and MyD88^(−/−) → MyD88^(−/−) (white bars) BM chimeric mice 10 h p.i. with 3 × 10⁷ conidia. Data are expressed as the fold change when compared to the WT → WT group and were pooled from 3 experiments with 12–15 mice per group. (C) BALF and (D) lung neutrophil recruitment in IL1R^(−/−) → WT (black circles), and WT → IL1R^(−/−) (white circles) BM chimeric mice 10 h p.i. with 3 × 10⁷ conidia. Data are expressed as mean (±SEM) and are from an experiment with 9 mice per group. (E-H) Mean (+SEM) BALF (E) neutrophil recruitment, (F) CXCL1, (G) CXCL2 and (H) CXCL5 levels, in MyD88^{(−/−) CC10-MyD88} (CC10-MyD88⁺; black bars) and in MyD88^(−/−) transgene-negative littermate controls (CC10-MyD88⁻; grey bars) 10 h p.i. with 3 × 10⁷ conidia. Data were pooled from 2 experiments and include 7–9 mice per genotype. (I) Kaplan-Meier survival plot of MyD88^(−/−) mice challenged with 6–7 × 10⁷ conidia and treated 4 h p.i. with 50 ng rCXCL1 (white circles, n = 11), or PBS vehicle (grey circles, n = 12). Data were pooled from 2 experiments (p = 0.026, Gehan-Breslow-Wilcoxon test).