PT  - JOURNAL ARTICLE
AU  - Jacobsen, Elizabeth
AU  - Sergei, Ochkur
AU  - Wen, Li
AU  - Zellner, Katie
AU  - Colbert, Dana
AU  - Protheroe, Cheryl
AU  - Lee, James
AU  - Lee, Nancy
TI  - Lung dysfunction in a mouse model of inflammation is dependent on T-cell-independent IL-13 expression (54.18)
DP  - 2011 Apr 01
TA  - The Journal of Immunology
PG  - 54.18--54.18
VI  - 186
IP  - 1 Supplement
4099  - http://www.jimmunol.org/content/186/1_Supplement/54.18.short
4100  - http://www.jimmunol.org/content/186/1_Supplement/54.18.full
SO  - J. Immunol.2011 Apr 01; 186
AB  - Chronic asthma is characterized by pulmonary remodeling and sustained lung dysfunction. The expression of IL-13 has been demonstrated as sufficient and necessary to induce these pathologies. Despite the common assumption that T cells are the primary source of IL-13 in the lung following allergen provocation, the mechanistic events leading to IL-13 expression are unclear, including the potential importance of other cells (i.e., non-T cells). Methods: Co-expression of IL-5 and eotaxin-2 induces pulmonary histopathologies and lung dysfunction that are eosinophil-dependent (i.e., they are absent in triple transgenic I5/hE2/PHIL) animals. IL-13 knockout and CD4 knockout mice were crossed with I5/hE2 mice to assess the effects of these deficiencies on the induced pathologies occurring in this double transgenic model. Conclusions: The Th2 pulmonary pathologies associated with I5/hE2 mice included recruitment of pulmonary effector T cells and increased brochoalveolar Th2 cytokine levels. Conversely, I5/hE2/CD4-/- had only a ~50% reduction in IL-13 levels as compared to I5/hE2 mice, suggesting that a significant portion of IL-13 is non-T cell derived in these mice. I5/hE2/IL-13-/- mice are improved in lung dysfunction and mucus production as compared to I5/hE2 mice. All mice had similar levels of eosinophil degranulation. These results demonstrate a role for non-T cell derived IL-13 that contributes to mucus production and lung dysfunction in a mouse model of chronic severe asthma.