Cow Dung Biomass Smoke Exposure Increases Adherence of Respiratory Pathogen Nontypeable Haemophilus influenzae to Human Bronchial Epithelial Cells

Cow Dung Biomass Smoke Exposure Increases Adherence of Respiratory Pathogen Nontypeable Haemophilus influenzae to Human Bronchial Epithelial Cells.

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Item Type: Article
Status: Published
Official URL: https://doi.org/10.1007/s12403-020-00351-y
Journal or Publication Title: Exposure and Health
Volume: 12
Number: 4
Page Range: pp. 883-895
Date: 2020
Divisions: UTS Centre for Inflammation
Depositing User: General Admin
Identification Number: 10.1007/s12403-020-00351-y
ISSN: 2451-9766
Date Deposited: 03 Jan 2021 23:58
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 effects 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 influenzae (NTHi), using immunofluorescence microscopy. In addition, expression of a known receptor of NTHi, platelet-activating factor receptor (PAFR), and two pro-inflammatory cytokines, interleukin 6 (IL-6) 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 wood-induced expression of PAFR and airway inflammatory 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.

Creators:
Creators
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KC, Rajendra
UNSPECIFIED
Hyland, Isabel K.
UNSPECIFIED
Smith, Jason A.
UNSPECIFIED
Shukla, Shakti D.
UNSPECIFIED
Hansbro, Philip M.
UNSPECIFIED
Zosky, Graeme R.
UNSPECIFIED
Karupiah, Gunasegaran
UNSPECIFIED
O’Toole, Ronan F.
UNSPECIFIED
Last Modified: 03 Jan 2021 23:58
URI: https://eprints.centenary.org.au/id/eprint/828

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