Eosinophils contribute to the resolution of lung-allergic responses following repeated allergen challenge - 05/02/15
Abstract |
Background |
Eosinophils accumulate at the site of allergic inflammation and are critical effector cells in allergic diseases. Recent studies have also suggested a role for eosinophils in the resolution of inflammation.
Objective |
To determine the role of eosinophils in the resolution phase of the response to repeated allergen challenge.
Methods |
Eosinophil-deficient (PHIL) and wild-type (WT) littermates were sensitized and challenged to ovalbumin (OVA) 7 or 11 times. Airway inflammation, airway hyperresponsiveness (AHR) to inhaled methacholine, bronchoalveolar lavage (BAL) cytokine levels, and lung histology were monitored. Intracellular cytokine levels in BAL leukocytes were analyzed by flow cytometry. Groups of OVA-sensitized PHIL mice received bone marrow from WT or IL-10−/− donors 30 days before the OVA challenge.
Results |
PHIL and WT mice developed similar levels of AHR and numbers of leukocytes and cytokine levels in BAL fluid after OVA sensitization and 7 airway challenges; no eosinophils were detected in the PHIL mice. Unlike WT mice, sensitized PHIL mice maintained AHR, lung inflammation, and increased levels of IL-4, IL-5, and IL-13 in BAL fluid after 11 challenges whereas IL-10 and TGF-β levels were decreased. Restoration of eosinophil numbers after injection of bone marrow from WT but not IL-10–deficient mice restored levels of IL-10 and TGF-β in BAL fluid as well as suppressed AHR and inflammation. Intracellular staining of BAL leukocytes revealed the capacity of eosinophils to produce IL-10.
Conclusions |
After repeated allergen challenge, eosinophils appeared not essential for the development of AHR and lung inflammation but contributed to the resolution of AHR and inflammation by producing IL-10.
Le texte complet de cet article est disponible en PDF.Key words : Eosinophils, resolution of inflammation, IL-10
Abbreviations used : AHR, BAL, EPO, MCh, OVA, PAS, PHIL, RL, TGF, WT
Plan
| This work was supported by the National Institutes of Health (grant no. HL-58723 to N.A.L., grant no. HL-065228 to J.J.L., and grant nos. AI-77609 and HL-36577 to E.W.G.). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Heart, Lung, and Blood Institute or the National Institutes of Health. |
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| Disclosure of potential conflict of interest: N. A. Lee and E. W. Gelfand have received research support from the National Institutes of Health. J. J. Lee has received research support from the National Institutes of Health, has received consultancy fees from AMGEN, has received payment for the development of educational presentations from Jackson Laboratory, and has received travel support to attend seminars. The rest of the authors declare that they have no relevant conflicts of interest. |
Vol 135 - N° 2
P. 451 - février 2015 Retour au numéro
Article précédent
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