Nasal epithelial barrier disruption by particulate matter ≤2.5 μm via tight junction protein degradation. Issue 5 (13th December 2017)

• Record Type: Journal Article
• Authors: Zhao, Renwu; Guo, Zhiqiang; Zhang, Ruxin; Deng, Congrui; Xu, Jian; Dong, Weiyang; Hong, Zhicong; Yu, Hongzhi; Situ, Huiru; Liu, Chunhui; Zhuang, Guoshun
• Is Part Of: Journal of applied toxicology. Volume 38:Issue 5(2018)
• Page Start: 678
• Page End: 687
• Publication Date: 2017-12-13
• Subjects: fine particulate matter (PM2.5) -- nasal epithelial cells -- nasal mucosa -- oxidative stress -- tight junctions; Toxicology -- Periodicals; Industrial toxicology -- Periodicals; Environmentally induced diseases -- Periodicals; Toxicology -- Periodicals; 615.9005
• DOI: 10.1002/jat.3573
• Languages: English
• ISSNs: 0260-437X

Abstract

Abstract: Upper airway diseases including sinonasal disorders may be caused by exposure to fine particulate matter (≤2.5 μm; PM2.5), as proven by epidemiological studies. PM2.5 is a complex entity whose chemical constituents and physicochemical properties are not confined to a single, independent "particle" but which in this study means a distinctive environmental "toxin." The mechanism whereby PM2.5 induces nasal epithelial barrier dysfunction leading to sinonasal pathology remains unknown. In the present study, human nasal epithelial cells were exposed to non‐cytotoxic doses of PM2.5 to examine how PM2.5 affects the nasal epithelial barrier. Tight junction (TJ) integrity and function were assessed by transepithelial electric resistance and paracellular permeability. The expression levels of TJ proteins such as zona occludens‐1, occludin and claudin‐1 were assessed by immunofluorescence staining and western blot. PM2.5 exposure induced epithelial barrier dysfunction as reflected by increased paracellular permeability and decreased transepithelial electric resistance. TJ proteins zona occludens‐1, occludin and claudin‐1 were found to be downregulated. Pretreatment with N ‐acetyl‐l ‐cysteine alleviated PM2.5‐mediated reactive oxygen species generation in RPMI 2650 cells, further preventing barrier dysfunction and attenuating the degradation of TJ proteins. These results suggest that PM2.5 induces nasal epithelial barrier disruption via oxidative stress, and N ‐acetyl‐l ‐cysteine counteracts this PM2.5‐mediated effect. Thus, nasal epithelial barrier disruption caused by PM2.5, which leads to sinonasal disease, may be prevented or treated through the inhibition of reactive oxygen species. Abstract : In this study, human nasal epithelial cells were exposed to non‐cytotoxic doses of particulate matter (≤2.5 μm; PM2.5) to examine how it affects the nasal epithelial barrier. The results showed that PM2.5 exposure induced epithelial barrier dysfunction as reflected by increased paracellular permeability and decreased transepithelial electric resistance. Tight junction proteins zona occludens‐1, occludin and claudin‐1 were found to be downregulated. Pretreatment with N ‐acetyl‐l ‐cysteine alleviated PM2.5‐mediated reactive oxygen species generation in nasal epithelial cells, further preventing barrier dysfunction and attenuating degradation of tight junction proteins.