Abstract
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.
Highlights
Asthma is a chronic inflammatory disease of the airways that reduces lung function and induces airway hyperresponsiveness (AHR) to nonspecific irritants [1, 2]
AHR is defined as an exacerbation of the airway responses towards stimulation, by a mechanism associated with a direct effect of inflammatory mediators on the airway smooth muscle and/or indirectly dependent on neural pathways or mast cell activation [3]
We examined the effects of alloxan-induced diabetes on a model of allergic lung inflammation triggered by OVA in sensitized mice
Summary
Asthma is a chronic inflammatory disease of the airways that reduces lung function and induces airway hyperresponsiveness (AHR) to nonspecific irritants [1, 2]. AHR is defined as an exacerbation of the airway responses towards stimulation, by a mechanism associated with a direct effect of inflammatory mediators on the airway smooth muscle and/or indirectly dependent on neural pathways or mast cell activation [3]. Different from allergic inflammatory responses, AHR does not depend exclusively on antigen activation and can result from nonspecific stimulation with irritants, including cold air, fumes or smoke, and particles [4, 5]. While several studies have shown a reduced incidence of asthma in type 1 diabetic patients [6, 7], others demonstrated an increased intercurrence between these diseases [8, 9]. In the works reporting a lower incidence of asthma in type 1 diabetic patients, the physiopathological mechanisms associated with this epidemiological profile are not yet fully understood [6, 7]
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