First Author | Kabbur PM | Year | 2006 |
Journal | Cell Immunol | Volume | 239 |
Issue | 1 | Pages | 67-74 |
PubMed ID | 16765924 | Mgi Jnum | J:110165 |
Mgi Id | MGI:3639535 | Doi | 10.1016/j.cellimm.2006.04.004 |
Citation | Kabbur PM, et al. (2006) Interleukin-10 does not mediate inhalational tolerance in a chronic model of ovalbumin-induced allergic airway disease. Cell Immunol 239(1):67-74 |
abstractText | OBJECTIVE: IL-10 is a potent anti-inflammatory cytokine, and IL-10-producing regulatory T cells are effective inhibitors of murine asthmatic responses. This study determined whether IL-10-dependent mechanisms mediated the local inhalational tolerance seen with chronic inhalational exposure to antigen. METHODS: Wildtype and IL-10(-/-) mice were sensitized with ovalbumin (OVA) and then challenged with daily OVA inhalations for 10 days or 6 weeks. RESULTS: The 10-day animals developed allergic airway disease, characterized by BAL eosinophilia, histologic airway inflammation and mucus secretion, methacholine hyperresponsiveness, and OVA-specific IgE production. These changes were more pronounced in IL-10(-/-) mice. The 6-week IL-10(-/-) and wildtype animals both developed inhalational tolerance, with resolution of airway inflammation but persistence of OVA-specific IgE production. CONCLUSION: IL-10 may have anti-inflammatory effects in the acute stage of murine allergic airways disease, but the cytokine does not mediate the development of local inhalational tolerance with chronic antigen exposure. |