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      Role of TNFR1 in the innate airway hyperresponsiveness of obese mice.

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          Abstract

          The purpose of this study was to examine the role of tumor necrosis factor receptor 1 (TNFR1) in the airway hyperresponsiveness characteristic of obese mice. Airway responsiveness to intravenous methacholine was measured using the forced oscillation technique in obese Cpe(fat) mice that were either sufficient or genetically deficient in TNFR1 (Cpe(fat) and Cpe(fat)/TNFR1(-/-) mice) and in lean mice that were either sufficient or genetically deficient in TNFR1 [wild-type (WT) and TNFR1(-/-) mice]. Compared with lean WT mice, Cpe(fat) mice exhibited airway hyperresponsiveness. Airway hyperresponsives was also greater in Cpe(fat)/TNFR1(-/-) than in Cpe(fat) mice. Compared with WT mice, Cpe(fat) mice had increases in bronchoalveolar lavage fluid concentrations of several inflammatory moieties including eotaxin, IL-9, IP-10, KC, MIG, and VEGF. These factors were also significantly elevated in Cpe(fat)/TNFR1(-/-) vs. TNFR1(-/-) mice. Additional moieties including IL-13 were also elevated in Cpe(fat)/TNFR1(-/-) vs. TNFR1(-/-) mice but not in Cpe(fat) vs. WT mice. IL-17A mRNA expression was greater in Cpe(fat)/TNFR1(-/-) vs. Cpe(fat) mice and in TNFR1(-/-) vs. WT mice. Analysis of serum indicated that obesity resulted in systemic as well as pulmonary inflammation, but TNFR1 deficiency had little effect on this systemic inflammation. Our results indicate that TNFR1 is protective against the airway hyperresponsiveness associated with obesity and suggest that effects on pulmonary inflammation may be contributing to this protection.

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          Author and article information

          Journal
          J. Appl. Physiol.
          Journal of applied physiology (Bethesda, Md. : 1985)
          American Physiological Society
          1522-1601
          0161-7567
          Nov 2012
          : 113
          : 9
          Affiliations
          [1 ] Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts 02115, USA.
          Article
          japplphysiol.00588.2012
          10.1152/japplphysiol.00588.2012
          3524665
          22984249
          5860f30f-3d37-4670-828f-35e733633136
          History

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