Down-regulation of mast cell activation and airway reactivity in diabetic rats: role of insulin

Abstract

Hormones play a modulating role in allergic inflammation. An inverse relationship between atopy and diabetes mellitus was reported. The mechanisms regulating this interaction are not completely understood. This study examined whether insulin influences mast cell activation following antigen challenge in rats.The experimental design included alloxan-induced diabetic rats and matching controls. Experiments were performed 30 days after alloxan injection. The animals were sensitised by s.c. injection of ovalbumin (OA) and aluminium hydroxide. OAinduced airway contraction, morphometric analysis of airway mast cells and tissue histamine quantification were evaluated in the isolated main bronchus and intrapulmonary bronchus upon exposure to antigen in vitro.Relative to controls, a reduced contraction to OA was observed in bronchial segments isolated from diabetic rats. This was accompanied by a 50% reduction in the number of degranulated mast cells and in histamine release. A complete recovery of the impaired responses was observed under the influence of insulin.In conclusion, the data suggested that insulin might modulate the controlling of mast cell degranulation; therefore, the early-phase response to antigen provocation, which represents a new insight into a better understanding of the mechanisms, accounted for the decreased risk of asthma among type-1 diabetic patients.

Synergistic effects of apelin and leptin on isolated rat pulmonary arteries

“…The protocol was repeated 2 weeks later [24]. In vitro challenge: After 7 days, before starting the administration of the studied substances, vascular rings were pre-treated with OVA (100 mg/mL).…”

Neutrophil function and metabolism in individuals with diabetes mellitus

“…These include decreased microvascular responses to inflammatory mediators such as histamine and bradykinin (3,4), decreased protein leakage and edema formation (5-7), reduced mast cell degranulation (8), decreased leukocyte-endothelial cell interactions and reduced number of leukocytes in inflammatory lesions (9)(10)(11)(12)(13)(14)(15), lowered airway inflammatory response to antigen challenge (16,17), low superoxide generation, and reduced release of tumor necrosis factor-α (TNF-α), interleukin-1ß and prostaglandin E 2 by leukocytes upon exposure to lipopolysaccharide (LPS) (18)(19)(20); low content of arachidonic acid in neutrophils (20), and a reduction in lymph node retention capacity (21). These abnormalities might contribute to the increased susceptibility and severity of infections in diabetic patients.…”

Insulin Inhibits LPS-Induced Signaling Pathways in Alveolar Macrophages

“…AMs (1x10 6 ) plated in 4-well tissue culture dishes were pre-treated or not with crystalline insulin at a final concentration of 1 mU/mL, 10 minutes before LPS stimulus in vitro [16]. Then, AMs were stimulated for 30 minutes with 100 ng/mL LPS and were placed on ice for 10 minutes to stop the reaction.…”