It was suggested that overproduction of proinflammatory cytokines (CXCL6 and interleukin 6 (IL-6)) from human PBMCs could be stimulated by the infection through activation of Toll-like receptor 4, nicotinamide adenine dinucleotide phosphate oxidase phosphatidylinositol 3-kinase and nuclear factor κB [24], at least as partial mechanisms by which PBMCs may be involved in the occurrence of AECOPD. This evidence concerns the gene IL6 and infection.