Respiratory syncytial virus-induced pulmonary disease and exacerbation of allergic asthma.
Several respiratory viruses have been shown to cause exacerbations of asthma. While the various viral responses likely have common mechanisms of activation, the respiratory syncytial virus (RSV) appears to promote specific responses that on their own can cause severe pulmonary problems. Understanding the mechanisms that promote inappropriate immune responses and local damage may lead to better therapy. The activation and recruitment of T cells that amplify and skew the immune response toward more intense pathology, including mucus production and remodeling of the airways, are likely scenarios that lead to more severe disease and clinical crisis in asthmatic patients. These mechanisms may also contribute to a significant proportion of exacerbations in chronic obstructive pulmonary disease. This review will focus on recent research on specific pathways of RSV-mediated activation of the innate host defense, including chemokine biology and TLR pathways, as well as on acquired immunity.
Department of Pathology, University of Michigan Medical School, Ann Arbor, Mich., USA.
Nicholas W
NW
Lukacs
Joost
J
Smit
Dennis
D
Lindell
Matthew
M
Schaller
D000818:Animals; D001249:Asthma / Q000276:immunology / Q000821:virology*; D018925:Chemokines / Q000276:immunology; D003713:Dendritic Cells / Q000276:immunology / Q000821:virology; D004195:Disease Models, Animal; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology; D051379:Mice; D009093:Mucus / Q000276:immunology / Q000821:virology; D018357:Respiratory Syncytial Virus Infections / Q000150:complications* / Q000276:immunology / Q000821:virology; D012136:Respiratory Syncytial Viruses / Q000276:immunology*; D051193:Toll-Like Receptors / Q000276:immunology
D018925:Chemokines; D051193:Toll-Like Receptors