Mouse models of rhinovirus-induced disease and exacerbation of allergic airway inflammation.
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.
Bartlett
Nathan W
NW
Department of Respiratory Medicine, UK National Heart and Lung Institute, and Medical Research Council & Asthma UK Centre in Allergic Mechanisms of Asthma, Imperial College London, Norfolk Place, London W2 1PG, UK.
Walton
Ross P
RP
Edwards
Michael R
MR
Aniscenko
Juliya
J
Caramori
Gaetano
G
Zhu
Jie
J
Glanville
Nicholas
N
Choy
Katherine J
KJ
Jourdan
Patrick
P
Burnet
Jerome
J
Tuthill
Tobias J
TJ
Pedrick
Michael S
MS
Hurle
Michael J
MJ
Plumpton
Chris
C
Sharp
Nigel A
NA
Bussell
James N
JN
Swallow
Dallas M
DM
Schwarze
Jurgen
J
Guy
Bruno
B
Almond
Jeffrey W
JW
Jeffery
Peter K
PK
Lloyd
Clare M
CM
Papi
Alberto
A
Killington
Richard A
RA
Rowlands
David J
DJ
Blair
Edward D
ED
Clarke
Neil J
NJ
Johnston
Sebastian L
SL
D000818:Animals; D000917:Antibody Formation / Q000528:radiation effects; D016535:Bronchial Hyperreactivity / Q000276:immunology / Q000821:virology; D018925:Chemokines / Q000096:biosynthesis / Q000276:immunology; D002630:Chemotactic Factors / Q000096:biosynthesis; D003713:Dendritic Cells / Q000276:immunology / Q000528:radiation effects; D004195:Disease Models, Animal; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology / Q000821:virology*; D007113:Immunity, Innate / Q000528:radiation effects; D007249:Inflammation; D018836:Inflammation Mediators / Q000276:immunology; D018799:Intercellular Adhesion Molecule-1 / Q000276:immunology; D051379:Mice; D008822:Mice, Transgenic; D009093:Mucus / Q000378:metabolism; D009504:Neutrophils / Q000276:immunology / Q000528:radiation effects; D010850:Picornaviridae Infections / Q000821:virology*; D012137:Respiratory System / Q000276:immunology / Q000473:pathology* / Q000528:radiation effects / Q000821:virology*; D012229:Rhinovirus / Q000502:physiology* / Q000528:radiation effects; D018417:Th1 Cells / Q000276:immunology / Q000528:radiation effects; D018418:Th2 Cells / Q000276:immunology / Q000528:radiation effects; D014466:Ultraviolet Rays; D038301:Virus Inactivation / Q000528:radiation effects; D014779:Virus Replication / Q000528:radiation effects
D018925:Chemokines; D002630:Chemotactic Factors; D018836:Inflammation Mediators; D018799:Intercellular Adhesion Molecule-1