PM2.5 aggravates airway inflammation in asthmatic mice: activating NF-κB via MyD88 signaling pathway

The role of PM2.5 in the bronchial asthma remains unclear. In this study, the deficient mice of TLR4-/-, TLR2-/- and MyD88 -/- were used to establish asthma model. The effects of PM2.5 on the inflammatory response in lung tissue of these mice were observed. PM2.5 increased alveolar macrophages and neutrophils, up-regulated the IL-12 and KC expression in WT mice, but down-regulated their levels in TLR2 -/-, TLR4 -/- and MyD88 -/- mice. OVA+PM2.5 stimulated neutrophil count in WT mice, but it decreased in TLR2 -/- and TLR4 -/- mice. OVA+PM2.5 also increased the Eotaxin, IL-5, IL-13 and MCP-3 expression levels, and OVA specific IgE and IgG1 in serum also increased in WT group. PM2.5 may activate NF-kappa B through the TLR2/TLR4/MyD88 signaling pathway and aggravate allergic inflammation of lung in asthmatic mice. The microelements in PM2.5 granules, such as lipopolysaccharide, may be an important factor in the high incidence of asthma.

Automated summary

This study observed the effects of PM2.5 on inflammatory response in lung tissue of deficient mice and found that PM2.5 may activate NF-κB through the TLR2/TLR4/MyD88 signaling pathway and exacerbate allergic inflammation in the lungs of asthmatic mice.