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Lookup NU author(s): Professor John SimpsonORCiD
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© 2014, BMJ Publishing Group. All rights reserved. Objectives: The observation that pathogenic bacteria are commonly tolerated in the human nose, yet drive florid inflammation in the lung, is poorly understood, partly due to limited availability of primary human cells from each location. We compared responses to bacterial virulence factors in primary human nasal and alveolar cells, and characterised the distribution of Tollinteracting protein (TOLLIP; an inhibitor of Toll-like receptor (TLR) signalling) in the human respiratory tract. Methods: Primary cells were isolated from nasal brushings and lung tissue taken from patients undergoing pulmonary resection. Cells were exposed to lipopolysaccharide, lipoteichoic acid, peptidoglycan, CpG-C DNA or tumour necrosis factor (TNF). Cytokines were measured in cell supernatants. TOLLIP was characterised using quantitative real-time PCR and immunofluorescence. Results: In primary alveolar, but not primary nasal, cells peptidoglycan significantly increased secretion of interleukin (IL)-1β, IL-6, IL-8, IL-10 and TNF. TLR2 expression was significantly higher in alveolar cells and correlated with IL-8 production. TOLLIP expression was significantly greater in nasal cells. Conclusion: In conclusion, primary human alveolar epithelial cells are significantly more responsive to peptidoglycan than primary nasal epithelial cells. This may partly be explained by differential TLR2 expression. TOLLIP is expressed widely in the human respiratory tract, and may contribute to the regulation of inflammatory responses.
Author(s): Moncayo-Nieto OL, Wilkinson TS, Brittan M, McHugh BJ, Jones RO, Morris AC, Walker WS, Davidson DJ, Simpson AJ
Publication type: Article
Publication status: Published
Journal: BMJ Open Respiratory Research
Year: 2014
Volume: 1
Issue: 1
Print publication date: 01/09/2014
Online publication date: 11/09/2014
Acceptance date: 27/07/2014
ISSN (electronic): 2052-4439
Publisher: BMJ Publishing Group
URL: https://doi.org/10.1136/bmjresp-2014-000046
DOI: 10.1136/bmjresp-2014-000046
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