PT  - JOURNAL ARTICLE
AU  - Olga Lucia Moncayo-Nieto
AU  - Thomas S Wilkinson
AU  - Mairi Brittan
AU  - Brian J McHugh
AU  - Richard O Jones
AU  - Andrew Conway Morris
AU  - William S Walker
AU  - Donald J Davidson
AU  - A John Simpson
TI  - Differential response to bacteria, and TOLLIP expression, in the human respiratory tract
AID  - 10.1136/bmjresp-2014-000046
DP  - 2014 Sep 01
TA  - BMJ Open Respiratory Research
PG  - e000046
VI  - 1
IP  - 1
4099  - http://bmjopenrespres.bmj.com/content/1/1/e000046.short
4100  - http://bmjopenrespres.bmj.com/content/1/1/e000046.full
SO  - BMJ Open Resp Res2014 Sep 01; 1
AB  - 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 Toll-interacting 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.