Cow dung biomass smoke exposure increases adherence of respiratory pathogen nontypeable Haemophilus infuenzae to human bronchial epithelial cells
KC, R and Hyland, IK and Smith, JA and Shukla, SD and Hansbro, PM and Zosky, GR and Karupiah, G and O'Toole, RF, Cow dung biomass smoke exposure increases adherence of respiratory pathogen nontypeable Haemophilus infuenzae to human bronchial epithelial cells, Exposure and Health ISSN 2451-9766 (2020) [Refereed Article]
Biomass smoke exposure is associated with a heightened risk of development of respiratory diseases that include chronic
obstructive pulmonary disease (COPD). The aim of this study was to increase our understanding of how biomass smoke
could contribute to an increased susceptibility to respiratory infection. We investigated the efects of cow dung and wood
smoke exposure on human bronchial epithelial cells with respect to adherence of a major respiratory bacterial pathogen in
COPD, nontypeable Haemophilus infuenzae (NTHi), using immunofuorescence microscopy. In addition, expression of a
known receptor of NTHi, platelet-activating factor receptor (PAFR), and two pro-infammatory cytokines, interleukin 6 (IL6) and interleukin-8 (IL-8), were determined using quantitative polymerase chain reaction. We observed a dose-dependent
increase in NTHi adhesion to human bronchial epithelial cells following exposure to cow dung but not wood smoke extracts.
Pre-treatment with PAFR antagonists, WEB-2086 and its analogue, C17, decreased adherence by NTHi to airway epithelial
cells exposed to cow dung smoke. Both cow dung and wood smoke-induced expression of PAFR, as well as of IL-6 and
IL-8, which was inhibited by WEB-2086 and C17. In conclusion, biomass smoke from combustion of cow dung and woodinduced expression of PAFR and airway infammatory markers in human bronchial epithelial cells. Cow dung exposure, but
not wood smoke exposure, mediated a measurable increase in NTHi adhesion to airway epithelial cells that was inhibited by
PAFR antagonists. This work highlights the potential of PAFR as a therapeutic target for reducing the impact of hazardous
biomass smoke exposure on respiratory health.