Figure 3.
CCR5 deficiency is associated with markedly increased expression of inflammatory cytokines and chemokines in the infarcted myocardium. A: Ribonuclease protection assay analysis demonstrated that CCR5-null mice show significantly higher peak mRNA expression of the proinflammatory cytokines TNF-α, IL-1β, and IL-6 (**P < 0.01, ***P < 0.001 versus wild-type [WT]) after 6 hours of reperfusion. B: Expression of the inhibitory cytokines IL-10 and TGF-β1 was also higher in CCR5-null infarcts when compared with wild-type animals (**P < 0.01 versus wild-type). C: The IL-1β:IL-10 and IL-1β:TGF-β1 expression ratio was significantly higher in CCR5-null infarcts (**P < 0.01 versus wild-type) indicating that CCR5 absence shifted the balance of cytokine expression toward increased proinflammatory activity. D: Expression of the chemokines MIP-1α, MIP-1β, and IP-10 was also significantly higher in CCR5-null infarcts (*P < 0.05, **P < 0.01 versus wild-type) after 6 hours of reperfusion. E: MIP-2 expression was markedly higher in CCR5−/− infarcts; however, MCP-1 levels were comparable between groups (n = 8 mice/group).