Toll-like receptor (TLR)-based networks regulate neutrophilic inflammation in respiratory disease

I. Sabroe*, M. K. B. Whyte

*Corresponding author for this work

Research output: Contribution to journalLiterature reviewpeer-review

Abstract

The neutrophil is a crucial early defence against microbial infection, but neutrophilic inflammation can result in devastating acute and chronic inflammatory diseases. In the lungs, the neutrophil is a principal part of the pathology of the acute respiratory distress syndrome, and its activation may also be of substantial importance in chronic obstructive pulmonary disease and some forms of asthma. induction of neutrophil recruitment in response to microbial attack requires activation of TLR (Toll-like receptor)-based signalling pathways and the concerted actions of multiple cell types, including sentinel cells such as monocytes and macrophages acting together with tissue cell types such as the epithelium or smooth-muscle cell. The present review describes some of these networks and the resulting potential for their targeting in respiratory disease.

Original languageEnglish
Pages (from-to)1492-1495
Number of pages4
JournalBiochemical Society Transactions
Volume35
DOIs
Publication statusPublished - Dec 2007

Keywords

  • lipopolysaccharide
  • lung
  • microbial infection
  • neutrophilic inflammation
  • respiratory disease
  • Toll-like receptor
  • AIRWAY SMOOTH-MUSCLE
  • OBSTRUCTIVE PULMONARY-DISEASE
  • INFLUENZA-A-VIRUS
  • EPITHELIAL-CELLS
  • ENDOTHELIAL-CELLS
  • SEVERE ASTHMA
  • INHALED ENDOTOXIN
  • CYSTIC-FIBROSIS
  • EXPRESSION
  • LIPOPOLYSACCHARIDE

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