title: Differential response to bacteria, and TOLLIP expression, in the human respiratory tract.
abstract: OBJECTIVE
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: University of Edinburgh/MRC Centre for Inflammation Research, University of Edinburgh , Edinburgh , UK ; Centre for Infectious Diseases, The Chancellor's Building, University of Edinburgh , Edinburgh , UK.
authors.forename: Olga Lucia
authors.initials: OL
authors.lastname: Moncayo-Nieto
authors.affiliation: Institute of Life Science, Medical Microbiology and Infectious Disease, Swansea University , Swansea , UK.
authors.forename: Thomas S
authors.initials: TS
authors.lastname: Wilkinson
authors.affiliation: University of Edinburgh/MRC Centre for Inflammation Research, University of Edinburgh , Edinburgh , UK.
authors.forename: Mairi
authors.initials: M
authors.lastname: Brittan
authors.affiliation: University of Edinburgh/MRC Centre for Inflammation Research, University of Edinburgh , Edinburgh , UK.
authors.forename: Brian J
authors.initials: BJ
authors.lastname: McHugh
authors.affiliation: University of Edinburgh/MRC Centre for Inflammation Research, University of Edinburgh , Edinburgh , UK.
authors.forename: Richard O
authors.initials: RO
authors.lastname: Jones
authors.affiliation: University of Edinburgh/MRC Centre for Inflammation Research, University of Edinburgh , Edinburgh , UK ; Department of Anaesthesia, University of Cambridge, Cambridge Biomedical Campus, Hills Road, Cambridge, UK.
authors.forename: Andrew
authors.initials: A
authors.lastname: Conway Morris
authors.affiliation: Department of Cardiothoracic Surgery , Royal Infirmary of Edinburgh , Edinburgh , UK.
authors.forename: William S
authors.initials: WS
authors.lastname: Walker
authors.affiliation: University of Edinburgh/MRC Centre for Inflammation Research, University of Edinburgh , Edinburgh , UK.
authors.forename: Donald J
authors.initials: DJ
authors.lastname: Davidson
authors.affiliation: University of Edinburgh/MRC Centre for Inflammation Research, University of Edinburgh , Edinburgh , UK ; Institute of Cellular Medicine, Newcastle University , Newcastle upon Tyne , UK.
authors.forename: A John
authors.initials: AJ
authors.lastname: Simpson
keywords: Innate Immunity