CXCL7-induced macrophage infiltration in lung tumor is independent of CXCR2 expression: CXCL7-induced macrophage chemotaxis in LLC tumors

Abstract Chemokinesplay diverse roles in modulating the immune response during tumor development. Levels of CXC chemokineligand 7 ( CXCL7) protein vary during tumorigenesis, and the evidence suggests that this chemokineserves as a novel biomarker of early-stage lung cancer. We investigated the effect of CXCL7gene expression on the infiltration of myeloid cells into the tumor microenvironmentin Lewis lung carcinoma(LLC). Tumors established from LLC cells overexpressing CXCL7( CXCL7-LLC tumors) increased the infiltration of CD206 + M2 macrophages at the early stages of tumorigenesis. This infiltration was independent of CXCR2 expression on either tumor cells or macrophages. CXCL7-LLC tumors developed faster than control-LLC tumors (IRES-LLC tumor) did. The extent of CD4 + T cell, CD8 + T cell, and natural killer T cellinfiltration was similar between the two tumor groups. Our findings suggest that CXCL7attracts macrophages especially at the tumor site and may accelerate lung tumor development in the early stages.