Production of other inflammatory cytokines was not altered by Cxcr2 deficiency. While the production of the chemokines CCL2 (a) and CCL5 (b) increased over 24 hours in injured mice compared to sham controls, no differences were noted between the strains (p = 0.963 and 0.090 for CCL2 and CCL5, respectively; two-way ANOVA effect of strain). Similarly, proinflammatory cytokines IL-1α, IL-1β, and TNFα (c, d, and e) were produced in response to CHI compared to sham controls (p b 0.05; two-way ANOVA effect of time); however, this response was similar in wild-type, Cxcr2 +/− , and Cxcr2 −/− mice. Lastly, the anti-inflammatory cytokine IL-10 (f) was not induced across the time course examined nor were there any differences detected between the three strains (p = 0.235 and 0.250; two-way ANOVA effect of time and strain, respectively). Data were expressed as mean + SEM; n = 4–6.