Objective To explore the effect of atmospheric fine particulate matter (PM_2.5) on the nuclear factor-kappa B (NF-κB) signaling pathway in rats with allergic rhinitis (AR).

Methods Forty specific pathogen-free male Wistar rats were divided into control group, AR group, AR+PM_2.5 group, and ammonium pyrrolidine dithiocarbamate (PDTC) group. Ovalbumin (OVA) sensitization was used to establish an AR model in the rats. The AR+PM_2.5 group and PDTC group were exposed to PM_2.5 via inhalation, the PDTC group was treated by intraperitoneal injection of PDTC at the same time, and the remaining groups were treated with an equivalent amount of normal saline. Behavioral indicators for AR were used for scoring; PAS staining was used to observe goblet cell proliferation in the nasal mucosa of the rats; scanning electron microscopy was used to observe the ultrastructure of the nasal mucosa of the rats; ELISA method was used to measure the content of IL-4, IL-5 and IL-6 in the nasal mucosa tissue of the rats; qRT-PCR assay was used to measure the mRNA expression levels of mucin 5AC (MUC5AC) and mouse calcium-activated chloride channel 3 (mCLCA3); Western blot was used to measure the protein expression levels of NF-κB p65 and IgE in the nasal mucosa of the rats.

Results Compared with the control group, the AR group and AR+PM_2.5 group had significantly increased AR scores, content of IL-4, IL-5 and IL-6, mRNA expression of MUC5AC and mCLCA3 and protein expression of NF-κB p65 and IgE (P < 0.05); meanwhile, the latter two groups showed more severe goblet cell proliferation and cilia destruction in the mucosa, with each indicator higher in the AR+PM_2.5 group than that in the AR group. After PDTC intervention, the PDTC group had significant improvement in all the above indicators compared with those in the AR+PM_2.5 group (P < 0.05).

Conclusion By activating the NF-κB signaling pathway, PM_2.5 increases the expression of downstream inflammation-related factors IL-4, IL-5, IL-6 and IgE, promotes the goblet cell proliferation in the nasal mucosa, and increases the expression of nasal mucus-related genes MUC5AC and mCLCA3, and thereby aggravates the pathological changes in the nasal mucosa and AR symptoms.