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Respiratory syncytial virus-induced CCL5/RANTES contributes to exacerbation of allergic airway inflammation.

Abstract
Severe respiratory syncytial virus (RSV) infection has a significant impact on airway function and may induce or exacerbate the response to a subsequent allergic challenge. In a murine model combining early RSV infection with later cockroach allergen (CRA) challenge, we examined the role of RSV-induced CCL5/RANTES production on allergic airway responses. RSV infection increased CCL5 mRNA and protein levels, peaking at days 8 and 12, respectively. Administration of CCL5 antiserum during days 0-14 of the RSV infection did not significantly alter viral protein expression when compared to mice treated with control serum. In mice receiving the combined RSV-allergen challenge, lungs collected on day 22 exhibited significantly increased numbers of CD4- and CD8-positive T cells. This increase in T cell numbers was not observed in mice receiving alpha-CCL5. On day 43, peribronchial eosinophilia and leukotriene levels were increased in RSV-allergen mice. Pretreatment with CCL5 antiserum resulted in decreased recruitment of inflammatory cells to bronchoalveolar and peribronchial regions of the lungs and these reductions were associated with a reduction in both T cell recruitment into the bronchoalveolar space, leukotriene release and chemokine generation. Thus, CCL5 released during RSV infection has a significant effect on the inflammatory response to subsequent allergic airway challenges.
AuthorsAlison E John, Aaron A Berlin, Nicholas W Lukacs
JournalEuropean journal of immunology (Eur J Immunol) Vol. 33 Issue 6 Pg. 1677-85 (Jun 2003) ISSN: 0014-2980 [Print] Germany
PMID12778486 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
Chemical References
  • Allergens
  • Chemokine CCL5
  • Chemokines
  • Immune Sera
  • Leukotrienes
  • Viral Proteins
Topics
  • Allergens (immunology)
  • Animals
  • Asthma (etiology)
  • Bronchi (immunology, pathology)
  • Bronchoalveolar Lavage Fluid (immunology)
  • CD4-Positive T-Lymphocytes (immunology)
  • CD8-Positive T-Lymphocytes (immunology)
  • Chemokine CCL5 (antagonists & inhibitors, biosynthesis, immunology, physiology)
  • Chemokines (biosynthesis)
  • Chemotaxis, Leukocyte
  • Cockroaches (immunology)
  • Eosinophilia (etiology)
  • Female
  • Flow Cytometry
  • Gene Expression Regulation, Viral
  • Humans
  • Immune Sera
  • Inflammation
  • Leukotrienes (metabolism)
  • Lung (immunology, pathology)
  • Mice
  • Mice, Inbred DBA
  • Models, Animal
  • Respiratory Hypersensitivity (etiology, physiopathology, prevention & control)
  • Respiratory Syncytial Virus Infections (complications, immunology, physiopathology)
  • Specific Pathogen-Free Organisms
  • Viral Proteins (biosynthesis)

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