Show simple item record

dc.contributor.authorKoth, Laura L
dc.contributor.authorRodriguez, Madeleine W
dc.contributor.authorBernstein, Xin Liu
dc.contributor.authorChan, Salina
dc.contributor.authorHuang, Xiaozhu
dc.contributor.authorCharo, Israel F
dc.contributor.authorRollins, Barrett Jon
dc.contributor.authorErle, David J
dc.date.accessioned2011-11-28T01:44:37Z
dc.date.issued2004
dc.identifier.citationKoth, Laura L., Madeleine W. Rodriguez, Xin Liu Bernstein, Salina Chan, Xiaozhu Huang, Israel F. Charo, Barrett J. Rollins, and David J. Erle. 2004. Aspergillus antigen induces robust Th2 cytokine production, inflammation, airway hyperreactivity and fibrosis in the absence of MCP-1 or CCR2. Respiratory Research 5(1): 12.en_US
dc.identifier.issn1465-9921en_US
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:5352098
dc.description.abstractBackground: Asthma is characterized by type 2 T-helper cell (Th2) inflammation, goblet cell hyperplasia, airway hyperreactivity, and airway fibrosis. Monocyte chemoattractant protein-1 (MCP-1 or CCL2) and its receptor, CCR2, have been shown to play important roles in the development of Th2 inflammation. CCR2-deficient mice have been found to have altered inflammatory and physiologic responses in some models of experimental allergic asthma, but the role of CCR2 in contributing to inflammation and airway hyperreactivity appears to vary considerably between models. Furthermore, MCP-1-deficient mice have not previously been studied in models of experimental allergic asthma. Methods: To test whether MCP-1 and CCR2 are each required for the development of experimental allergic asthma, we applied an Aspergillus antigen-induced model of Th2 cytokine-driven allergic asthma associated with airway fibrosis to mice deficient in either MCP-1 or CCR2. Previous studies with live Aspergillus conidia instilled into the lung revealed that MCP-1 and CCR2 play a role in anti-fungal responses; in contrast, we used a non-viable Aspergillus antigen preparation known to induce a robust eosinophilic inflammatory response. Results: We found that wild-type C57BL/6 mice developed eosinophilic airway inflammation, goblet cell hyperplasia, airway hyperreactivity, elevations in serum IgE, and airway fibrosis in response to airway challenge with Aspergillus antigen. Surprisingly, mice deficient in either MCP-1 or CCR2 had responses to Aspergillus antigen similar to those seen in wild-type mice, including production of Th2 cytokines. Conclusion: We conclude that robust Th2-mediated lung pathology can occur even in the complete absence of MCP-1 or CCR2.en_US
dc.language.isoen_USen_US
dc.publisherBioMed Centralen_US
dc.relation.isversionofdoi:10.1186/1465-9921-5-12en_US
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC520828/pdf/en_US
dash.licenseLAA
dc.titleAspergillus Antigen Induces Robust Th2 Cytokine Production, Inflammation, Airway Hyperreactivity and Fibrosis in the Absence of MCP-1 or CCR2en_US
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden_US
dc.relation.journalRespiratory Researchen_US
dash.depositing.authorRollins, Barrett Jon
dc.date.available2011-11-28T01:44:37Z
dash.affiliation.otherHMS^Medicine-Brigham and Women's Hospitalen_US
dc.identifier.doi10.1186/1465-9921-5-12*
dash.contributor.affiliatedRollins, Barrett


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record