Mast Cell-Deficient KitW-sh Mice Develop House Dust Mite-Induced Lung Inflammation despite Impaired Eosinophil Recruitment

Background: Mast cells are implicated in allergic and innate immune responses in asthma, although their role in models using an allergen relevant for human disease is incompletely understood. House dust mite (HDM) allergy is common in asthma patients. Our aim was to investigate the role of mast cell...

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Veröffentlicht in:Journal of innate immunity 2013-10, Vol.6 (2), p.219-226
Hauptverfasser: de Boer, J. Daan, Yang, Jack, van den Boogaard, Florry E., Hoogendijk, Arie J., de Beer, Regina, van der Zee, Jaring S., Roelofs, Joris J.T.H., van 't Veer, Cornelis, de Vos, Alex F., van der Poll, Tom
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Sprache:eng
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Zusammenfassung:Background: Mast cells are implicated in allergic and innate immune responses in asthma, although their role in models using an allergen relevant for human disease is incompletely understood. House dust mite (HDM) allergy is common in asthma patients. Our aim was to investigate the role of mast cells in HDM-induced allergic lung inflammation. Methods: Wild-type (Wt) and mast cell-deficient Kit w-sh mice on a C57BL/6 background were repetitively exposed to HDM via the airways. Results: HDM challenge resulted in a rise in tryptase activity in bronchoalveolar lavage fluid (BALF) of Wt mice, indicative of mast cell activation. Kit w-sh mice showed a strongly attenuated HDM- induced recruitment of eosinophils in BALF and lung tissue, accompanied by reduced pulmonary levels of the eosinophil chemoattractant eotaxin. Remarkably, Kit w-sh mice demonstrated an unaltered capacity to develop lung pathology and increased mucus production in response to HDM. The increased plasma IgE in response to HDM in Wt mice was absent in Kit w-sh mice. Conclusion: These data contrast with previous reports on the role of mast cells in models using ovalbumin as allergen in that C57BL/6 Kit w-sh mice display a selective impairment of eosinophil recruitment without differences in other features of allergic inflammation.
ISSN:1662-811X
1662-8128
DOI:10.1159/000354984