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CD49d-expressing neutrophils differentiate atopic from nonatopic individuals

Several epidemiologic studies have demonstrated that severe respiratory viral infections markedly increase the risk of atopic disease including asthma.1,2 By using a Sendai virus (SeV) mouse model, we previously demonstrated a mechanistic pathway leading from viral infection to atopic disease that w...

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Bibliographic Details
Published in:Journal of allergy and clinical immunology 2014-03, Vol.133 (3), p.901-904.e5
Main Authors: Sigua, Jerome A., MD, Buelow, Becky, MD, Cheung, Dorothy S., MD, Buell, Erika, BS, Hunter, Desire, BS, Klancnik, Meribeth, MLT, Grayson, Mitchell H., MD
Format: Article
Language:English
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Summary:Several epidemiologic studies have demonstrated that severe respiratory viral infections markedly increase the risk of atopic disease including asthma.1,2 By using a Sendai virus (SeV) mouse model, we previously demonstrated a mechanistic pathway leading from viral infection to atopic disease that was dependent on the initial recruitment of CD49d-expressing neutrophils3 (CD49d+ PMN) to the airway.4-6 Although we have documented that parts of this pathway are intact in human beings,7-9 whether or not CD49d+ PMN are found in human atopic disease has not been described previously. [...]we sought to determine whether proatopic CD49d+ PMN were preferentially found in the blood and/or nasal lavage of subjects with atopy and whether they would be recruited to the nasal mucosa in response to an allergen challenge. Nonetheless, our findings begin to illuminate potential mechanisms that may be involved in the development or maintenance of allergic disease in humans.\n For the irrelevant allergen, we chose an allergen to which the subject did not have a reaction but was of a similar seasonality as the relevant allergen (eg, a dust mite monosensitized individual would be challenged with cat and a timothy grass monosensitized subject would be challenged with Bermuda grass).
ISSN:0091-6749
1097-6825
DOI:10.1016/j.jaci.2013.09.035