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Differential response to bacteria, and TOLLIP expression, in the human respiratory tract
  1. Olga Lucia Moncayo-Nieto1,2,
  2. Thomas S Wilkinson3,
  3. Mairi Brittan1,
  4. Brian J McHugh1,
  5. Richard O Jones1,
  6. Andrew Conway Morris1,4,
  7. William S Walker5,
  8. Donald J Davidson1 and
  9. A John Simpson1,6
  1. 1University of Edinburgh/MRC Centre for Inflammation Research, University of Edinburgh, Edinburgh, UK
  2. 2Centre for Infectious Diseases, The Chancellor's Building, University of Edinburgh, Edinburgh, UK
  3. 3Institute of Life Science, Medical Microbiology and Infectious Disease, Swansea University, Swansea, UK
  4. 4Department of Anaesthesia, University of Cambridge, Cambridge Biomedical Campus, Hills Road, Cambridge, UK
  5. 5Department of Cardiothoracic Surgery, Royal Infirmary of Edinburgh, Edinburgh, UK
  6. 6Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK
  1. Correspondence to Prof A John Simpson; j.simpson{at}ncl.ac.uk

Abstract

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.

  • Innate Immunity

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