Thus, reduction of circulating CXCL5 appears to improve host defense to bacterial infection perhaps by allowing proper scavenging of other chemokines (keratinocyte-derived chemokine [KC or CXCL1] and macrophage inflammatory protein 2-alpha [MIP2-α or CXCL2]), allowing the formation of chemokine gradients and sensitizing CXCR2, resulting in an increased influx of neutrophils (41). The gene discussed is CXCL1; the disease is bacterial infectious disease.