Advanced Role of Neutrophils in Common Respiratory Diseases

Figure 2

a: infection of virus can stimulate airway epithelium and produce antimicrobiota defense through IL-22/IL-22R signaling pathway. b: the colonization of bacterial pathogens could cause the release of IL-8/IL-6/TNF-α/IFN-γ. c1: cigarette smoking (CS) could induce the release of damage-associated molecular patterns (DAMPs). DAMPs can activate the innate immune system by binding to pattern recognition receptors (PRRs), such as TLR2, TLR4, and TLR9, and further induce CXCL8 release via TLR9 activation. c2: CS increase the expression of both p50 and p65 subunits of NF-kappaB in neutrophils and reduce the spontaneous apoptosis of neutrophils. c3: CS could cause the degranulation of secondary granules. This contributes to the accumulation of neutrophils and inflammation within the airways of smokers. c4: the efferocytosis damage caused by CS can increase the release of proteases and elastases. It not only impairs the antimicrobial defense but also (d) promotes the pulmonary inflammation and tissue degradation.