Airway smooth muscle and immunomodulation in acute exacerbations of airway disease

Immunol Rev. 2011 Jul;242(1):178-85. doi: 10.1111/j.1600-065X.2011.01022.x.

Abstract

Airway smooth muscle (ASM) manifests a hyperresponsive phenotype in airway disorders such as asthma, chronic obstructive pulmonary disease (COPD), and cystic fibrosis. Current evidence also suggests that ASM modulates immune responses by secreting mediators and expressing cell surface molecules. Such processes amplify or dampen inflammation by inflammatory cells in the airways or by altering cellular responses to viruses, bacteria, or pathogens known to exacerbate airways diseases.

Publication types

  • Review

MeSH terms

  • Airway Remodeling / immunology*
  • Allergens / immunology
  • Animals
  • Asthma / immunology
  • Asthma / physiopathology
  • Child
  • Cystic Fibrosis / immunology
  • Cystic Fibrosis / physiopathology
  • Epithelial Cells / immunology*
  • Epithelial Cells / metabolism
  • Humans
  • Hypersensitivity / immunology*
  • Hypersensitivity / physiopathology
  • Immunity, Innate*
  • Immunomodulation*
  • Inflammation / immunology
  • Interleukin-33
  • Interleukins / biosynthesis
  • Interleukins / immunology
  • Mice
  • Mice, Transgenic
  • Muscle, Smooth / immunology*
  • Muscle, Smooth / metabolism
  • Pulmonary Disease, Chronic Obstructive / immunology
  • Pulmonary Disease, Chronic Obstructive / physiopathology
  • Respiratory System / immunology*
  • Respiratory System / physiopathology
  • Signal Transduction / immunology
  • Toll-Like Receptor 4 / immunology
  • Toll-Like Receptor 4 / metabolism
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Tumor Necrosis Factor-alpha / immunology

Substances

  • Allergens
  • IL33 protein, human
  • Interleukin-33
  • Interleukins
  • TLR4 protein, human
  • Toll-Like Receptor 4
  • Tumor Necrosis Factor-alpha