In turn, antibodies to the platelet-derived chemokines CCL5 and CXCL4, pharmacological disruption of the CCL5-CXCL4 heteromers or, neutralization of CCR5 diminish lung edema, neutrophil infiltration, and tissue damage in LPS-,acid- and sepsis-induced ALI [16]. This evidence concerns the gene PF4 and Sepsis.