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Mediators of Inflammation
Volume 2018 (2018), Article ID 6150843, 11 pages
Research Article

Diabetes Downregulates Allergen-Induced Airway Inflammation in Mice

1Laboratory of Inflammation, Oswaldo Cruz Institute, FIOCRUZ, Av. Brasil No. 4365, 21045-900 Manguinhos, RJ, Brazil
2Federal University of Alagoas, 57072-970 Maceió, AL, Brazil
3Cedars-Sinai Medical Center, 8700 Beverly Blvd, Los Angeles, CA 90048, USA

Correspondence should be addressed to PatrĂ­cia M. R. Silva; moc.liamg@0191avlistap

Received 24 November 2017; Accepted 20 February 2018; Published 15 April 2018

Academic Editor: Sonya Marshall-Gradisnik

Copyright © 2018 Vinicius F. Carvalho et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Previous studies described that allergic diseases, including asthma, occur less often than expected in patients with type 1 diabetes. Here, we investigated the influence of diabetes on allergic airway inflammation in a model of experimental asthma in mice. Diabetes was induced by intravenous injection of alloxan into 12 h-fasted A/J mice, followed by subcutaneous sensitization with ovalbumin (OVA) and aluminum hydroxide (Al(OH)3), on days 5 and 19 after diabetes induction. Animals were intranasally challenged with OVA (25 μg), from day 24 to day 26. Alloxan-induced diabetes significantly attenuated airway inflammation as attested by the lower number of total leukocytes in the bronchoalveolar lavage fluid, mainly neutrophils and eosinophils. Suppression of eosinophil infiltration in the peribronchiolar space and generation of eosinophilotactic mediators, such as CCL-11/eotaxin, CCL-3/MIP-1α, and IL-5, were noted in the lungs of diabetic sensitized mice. In parallel, reduction of airway hyperreactivity (AHR) to methacholine, mucus production, and serum IgE levels was also noted under diabetic conditions. Our findings show that alloxan diabetes caused attenuation of lung allergic inflammatory response in A/J mice, by a mechanism possibly associated with downregulation of IgE antibody production.