Advanced Role of Neutrophils in Common Respiratory Diseases

Figure 1

a: microbial component and environmental allergens such as LPS and β-glucan could recruit neutrophils via TLR-4/CXCR-2/MD2 and dectin-1. The recruited neutrophils could produce ROS/leukotrienes/IL-33/TSLP and cause inflammation or sensitization. b: the foreign allergens can act on airway epithelium and induce neutrophils to release CXCL8/NE/MMP-9, which is mediated by TLR-7/8. The released substance could amplify the recruitment of neutrophils in a positive feedback manner. c: microbial products and inhaled allergens can induce Th17 activated through TIRF and MYD88 by activating IRF-3, inducing I interferons, upregulating CD40 on DC, and finally releasing IL-6 and IL-1β to act towards airway neutrophils. TIRF also contribute to Th17 responses to inhaled allergens by increasing recruitment of DCs and to drive Th17 cell differentiation. d: HDM-DP could induce the secretion of S100A8/S100A9. The combination of S100A8/S100A9 might activate TLR4/Lyn/PI3K/Akt/ERK/NF-kappaB pathway to produce an antiapoptotic effect on neutrophils. e: the stimulated or survival neutrophils can cause the persistence of inflammation. As a result, the lung function is getting poorer and poorer.