Figure 6.
Figure 6. Administration of recombinant CXCL2 and CXCL5 rescues the impaired host defense seen in Cxcl1−/− mice during pneumococcal lung infection. (A-H) WT and Cxcl1−/− mice were infected intratracheally with S pneumoniae 6303 (5 × 104 CFU). Mice were treated with murine recombinant CXCL2 and CXCL5 intratracheally at 1-hour postinfection and then euthanized at 48 hours postinfection. BALF neutrophil counts (A) and bacterial burden in lungs (B) and spleen (C) were quantitated. BALF neutrophil counts (D) and bacterial burden in lungs (E) and spleen (F) were quantitated. FACS dot plot (G) and mature neutrophil (subpopulation #5; Ly6G+c-Kit−) counts in bone marrow (H) were measured. (n = 5-6 mice/infection group; n = 3 mice/control group). All experiments were performed 3 times. Statistical significance was determined by 1-way ANOVA (followed by Bonferroni’s post hoc comparisons; A-H). *P < .05; **P < .01.

Administration of recombinant CXCL2 and CXCL5 rescues the impaired host defense seen in Cxcl1−/−mice during pneumococcal lung infection. (A-H) WT and Cxcl1−/− mice were infected intratracheally with S pneumoniae 6303 (5 × 104 CFU). Mice were treated with murine recombinant CXCL2 and CXCL5 intratracheally at 1-hour postinfection and then euthanized at 48 hours postinfection. BALF neutrophil counts (A) and bacterial burden in lungs (B) and spleen (C) were quantitated. BALF neutrophil counts (D) and bacterial burden in lungs (E) and spleen (F) were quantitated. FACS dot plot (G) and mature neutrophil (subpopulation #5; Ly6G+c-Kit) counts in bone marrow (H) were measured. (n = 5-6 mice/infection group; n = 3 mice/control group). All experiments were performed 3 times. Statistical significance was determined by 1-way ANOVA (followed by Bonferroni’s post hoc comparisons; A-H). *P < .05; **P < .01.

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