The antibody treatment exerted anti-inflammatory effects via simultaneous inhibition of IL-6, CXCL8/IL-8, CCL3/MIP-1, TNF-α, and IFN-γ production, and had direct and considerable suppressive effects on excessive CCL and CXCL gene expression associated with sepsis immunopathogenesis (Mei et al, 2010; Mercer et al, 2014; Paudel et al, 2019; Shalova et al, 2015; Souto et al, 2011). This evidence concerns the gene CCL3 and Sepsis.