Mouse models of rhinovirus-induced disease and exacerbation of allergic airway inflammation

Nat Med. 2008 Feb;14(2):199-204. doi: 10.1038/nm1713. Epub 2008 Feb 3.

Abstract

Rhinoviruses cause serious morbidity and mortality as the major etiological agents of asthma exacerbations and the common cold. A major obstacle to understanding disease pathogenesis and to the development of effective therapies has been the lack of a small-animal model for rhinovirus infection. Of the 100 known rhinovirus serotypes, 90% (the major group) use human intercellular adhesion molecule-1 (ICAM-1) as their cellular receptor and do not bind mouse ICAM-1; the remaining 10% (the minor group) use a member of the low-density lipoprotein receptor family and can bind the mouse counterpart. Here we describe three novel mouse models of rhinovirus infection: minor-group rhinovirus infection of BALB/c mice, major-group rhinovirus infection of transgenic BALB/c mice expressing a mouse-human ICAM-1 chimera and rhinovirus-induced exacerbation of allergic airway inflammation. These models have features similar to those observed in rhinovirus infection in humans, including augmentation of allergic airway inflammation, and will be useful in the development of future therapies for colds and asthma exacerbations.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibody Formation / radiation effects
  • Bronchial Hyperreactivity / immunology
  • Bronchial Hyperreactivity / virology
  • Chemokines / biosynthesis
  • Chemokines / immunology
  • Chemotactic Factors / biosynthesis
  • Dendritic Cells / immunology
  • Dendritic Cells / radiation effects
  • Disease Models, Animal*
  • Humans
  • Hypersensitivity / immunology
  • Hypersensitivity / virology*
  • Immunity, Innate / radiation effects
  • Inflammation
  • Inflammation Mediators / immunology
  • Intercellular Adhesion Molecule-1 / immunology
  • Mice
  • Mice, Transgenic
  • Mucus / metabolism
  • Neutrophils / immunology
  • Neutrophils / radiation effects
  • Picornaviridae Infections / virology*
  • Respiratory System / immunology
  • Respiratory System / pathology*
  • Respiratory System / radiation effects
  • Respiratory System / virology*
  • Rhinovirus / physiology*
  • Rhinovirus / radiation effects
  • Th1 Cells / immunology
  • Th1 Cells / radiation effects
  • Th2 Cells / immunology
  • Th2 Cells / radiation effects
  • Ultraviolet Rays
  • Virus Inactivation / radiation effects
  • Virus Replication / radiation effects

Substances

  • Chemokines
  • Chemotactic Factors
  • Inflammation Mediators
  • Intercellular Adhesion Molecule-1