title: Influence of respiratory syncytial virus infection on cytokine and inflammatory responses in allergic mice.
abstract: BACKGROUND
  Th2 lymphocyte responses are associated with inflammation and disease during allergic responses. Exposure to particular environmental factors during the expression of allergy could result in more pronounced Th2-like immune responses and more severe disease. One factor might be a respiratory virus infection.
  
  
  OBJECTIVE
  The aim of our study was to investigate the influence of respiratory syncytial virus (RSV) infection on the expression of ovalbumin (OVA)-induced allergy in BALB/c mice.
  
  
  METHODS
  We determined OVA-specific IgE in serum, cytokine profiles and histopathological lesions in lungs of OVA-allergic mice after RSV infection.
  
  
  RESULTS
  OVA sensitization and challenge induced OVA-specific IgE in serum, Th2 cytokine mRNA expression, and mononuclear and eosinophilic inflammation in the lungs. RSV inoculation during the challenge period enhanced OVA-induced IL-4 and IL-5 mRNA expression in lung tissue. RSV further enhanced the OVA-induced hypertrophy of mucous cells and eosinophilic infiltration in lung tissue. Surprisingly, RSV infection decreased Th2 cytokine secretion and eosinophilic influx in bronchoalveolar lavage of OVA-allergic mice. Because inactivated RSV did not influence these responses, replication of RSV appeared essential for the modification of OVA-induced Th2 cytokine expression. RSV did not change OVA-specific IgE levels in serum. Furthermore, the RSV-induced IL-12 mRNA expression in lung tissue of OVA-allergic mice was diminished, but IFN-gamma mRNA expression was not affected.
  
  
  CONCLUSIONS
  RSV infection enhanced particular OVA-induced Th2 cytokine mRNA responses and pulmonary lesions in allergic mice and thus aggravated allergic respiratory disease.
authors.affiliation: Research Laboratory for Infectious Diseases, National Institute of Public Health and the Environment, Bilthoven, The Netherlands. marion.barends@rivm.nl
authors.forename: M
authors.initials: M
authors.lastname: Barends
authors.forename: A
authors.initials: A
authors.lastname: Boelen
authors.forename: L
authors.initials: L
authors.lastname: de Rond
authors.forename: J
authors.initials: J
authors.lastname: Kwakkel
authors.forename: T
authors.initials: T
authors.lastname: Bestebroer
authors.forename: J
authors.initials: J
authors.lastname: Dormans
authors.forename: H
authors.initials: H
authors.lastname: Neijens
authors.forename: T
authors.initials: T
authors.lastname: Kimman
mesh_terms: D000818:Animals; D000918:Antibody Specificity / Q000276:immunology; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology; D016207:Cytokines / Q000096:biosynthesis* / Q000276:immunology*; D004195:Disease Models, Animal; D005260:Female; D006967:Hypersensitivity / Q000276:immunology / Q000503:physiopathology; D007073:Immunoglobulin E / Q000097:blood / Q000276:immunology; D008168:Lung / Q000098:blood supply / Q000166:cytology / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin / Q000009:adverse effects / Q000276:immunology; D011014:Pneumonia / Q000276:immunology* / Q000503:physiopathology*; D012333:RNA, Messenger / Q000096:biosynthesis / Q000276:immunology; D018357:Respiratory Syncytial Virus Infections / Q000276:immunology* / Q000503:physiopathology*; D018113:Respiratory Syncytial Virus, Human; D012720:Severity of Illness Index; D013997:Time Factors; D014466:Ultraviolet Rays
chemical_list: D016207:Cytokines; D012333:RNA, Messenger; D007073:Immunoglobulin E; D010047:Ovalbumin