title: Enhanced allergic responsiveness after early childhood infection with respiratory viruses: Are long-lived alternatively activated macrophages the missing link?
abstract: Early childhood infection with respiratory viruses, including human rhinovirus, respiratory syncytial virus (RSV) and influenza, is associated with an increased risk of allergic asthma and severe exacerbation of ongoing disease. Despite the long recognition of this relationship, the mechanism linking viral infection and later susceptibility to allergic lung inflammation is still poorly understood. We discuss the literature and provide new evidence demonstrating that these viruses induce the alternative activation of macrophages. Alternatively activated macrophages (AAM) induced by RSV or influenza infection persisted in the lungs of mice up to 90 days after initial viral infection. Several studies suggest that AAM contribute to allergic inflammatory responses, although their mechanism of action is unclear. In this commentary, we propose that virus-induced AAM provide a link between viral infection and enhanced responses to inhaled allergens.
authors.affiliation: Department of Microbiology and Immunology, University of Maryland School of Medicine, 685 W. Baltimore St., Rm 380, Baltimore, MD 21201, USA Research and Development Service, Department of Veterans Affairs, VA Maryland Health Care System, Baltimore, MD 21201, USA akeegan@som.umaryland.edu.
authors.forename: Achsah D
authors.initials: AD
authors.lastname: Keegan
authors.affiliation: Department of Microbiology and Immunology, University of Maryland School of Medicine, 685 W. Baltimore St., Rm 380, Baltimore, MD 21201, USA.
authors.forename: Kari Ann
authors.initials: KA
authors.lastname: Shirey
authors.affiliation: Department of Pediatrics, University of Maryland School of Medicine, 29 South Greene St., Suite 1000, Baltimore, MD 21201, USA.
authors.forename: Dayanand
authors.initials: D
authors.lastname: Bagdure
authors.affiliation: Department of Research and Development, Sigmovir Biosystems, Inc., 9650 Medical Center Drive, Rockville, MD 20850, USA.
authors.forename: Jorge
authors.initials: J
authors.lastname: Blanco
authors.affiliation: Department of Pediatrics, University of Maryland School of Medicine, 29 South Greene St., Suite 1000, Baltimore, MD 21201, USA.
authors.forename: Rose M
authors.initials: RM
authors.lastname: Viscardi
authors.affiliation: Department of Microbiology and Immunology, University of Maryland School of Medicine, 685 W. Baltimore St., Rm 380, Baltimore, MD 21201, USA.
authors.forename: Stefanie N
authors.initials: SN
authors.lastname: Vogel
mesh_terms: D000818:Animals; D001249:Asthma / Q000453:epidemiology / Q000209:etiology; D002648:Child; D002675:Child, Preschool; D018450:Disease Progression; D006801:Humans; D006967:Hypersensitivity / Q000453:epidemiology* / Q000209:etiology*; D008262:Macrophage Activation / Q000276:immunology; D008264:Macrophages / Q000276:immunology / Q000378:metabolism / Q000821:virology; D012141:Respiratory Tract Infections / Q000150:complications* / Q000276:immunology / Q000821:virology*; D012306:Risk
keywords: Th2 cytokines; allergic asthma; alternatively activated macrophages; respiratory virus infection