Diabetes Downregulates Allergen-Induced Airway Inflammation in Mice.
Vinicius de Frias CarvalhoEmiliano O BarretoAna Carolina S ArantesMagda F SerraTatiana Paula T FerreiraYago A P Jannini-SáCory M HogaboamMarco A MartinsPatrícia M R SilvaPublished in: Mediators of inflammation (2018)
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.
Keyphrases
- type diabetes
- cardiovascular disease
- glycemic control
- high fat diet induced
- allergic rhinitis
- inflammatory response
- chronic obstructive pulmonary disease
- insulin resistance
- high glucose
- wild type
- diabetic rats
- high dose
- adipose tissue
- gold nanoparticles
- low dose
- metabolic syndrome
- cystic fibrosis
- toll like receptor
- atomic force microscopy
- stress induced