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Cow dung biomass smoke exposure increases adherence of respiratory pathogen nontypeable Haemophilus infuenzae to human bronchial epithelial cells

Citation

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]

Copyright Statement

Springer Nature B.V. 2020

DOI: doi:10.1007/s12403-020-00351-y

Abstract

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.

Item Details

Item Type:Refereed Article
Keywords:chronic obstructive pulmonary disease, cow dung smoke, biomass smoke, cigarette smoke, nontypeable, <i>Haemophilus infuenzae</i>
Research Division:Biomedical and Clinical Sciences
Research Group:Cardiovascular medicine and haematology
Research Field:Respiratory diseases
Objective Division:Health
Objective Group:Clinical health
Objective Field:Clinical health not elsewhere classified
UTAS Author:KC, R (Mr Rajendra KC)
UTAS Author:Hyland, IK (Ms Isabel Hyland)
UTAS Author:Smith, JA (Associate Professor Jason Smith)
UTAS Author:Zosky, GR (Professor Graeme Zosky)
UTAS Author:Karupiah, G (Associate Professor Guna Karupiah)
UTAS Author:O'Toole, RF (Dr Ronan O'Toole)
ID Code:139796
Year Published:2020
Web of Science® Times Cited:4
Deposited By:Medicine
Deposited On:2020-07-06
Last Modified:2020-08-20
Downloads:0

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