Airway inflammatory events in diabetic-antigen sensitized guinea pigs.

Experimental evidence indicates that the relative lack of insulin in an organism results in an overall reduction in inflammatory reactions. This study was planned to determine the inflammatory events in antigen sensitized diabetic guinea pigs. Twenty-five male guinea pigs were categorized into five groups of five each as follows: diabetic, antigen sensitized, antigen sensitized diabetic, insulin-treated antigen sensitized diabetic and control animals. Induction of experimental diabetes and antigen sensitization was performed by injection of streptozotocin and ovalbumin, respectively. Animals were killed by exsanguination and bronchoalveolar lavage was performed. Bronchoalveolar lavage fluid cellular and protein contents were determined. Airway responsiveness to acetylcholine was assessed using isolated tracheal triple-ring. Histopathological examinations were performed on the lungs. Decreases in the airway reactivity in diabetic and antigen sensitized diabetic animals were found compared with antigen sensitized animals. Experimental diabetes also decreased antigen-induced protein leakage into the airspace as well as the accumulation of inflammatory cells (eosinophils, neutrophils, lymphocytes and macrophages) in bronchoalveolar lavage fluid of antigen sensitized animals. Insulin treatment prevented these decreases in protein content and inflammatory cells infiltration in bronchoalveolar lavage fluid observed in the antigen sensitized guinea pigs with diabetes. Histopathological results showed that coinduction of experimental diabetes significantly reduces the number of eosinophils in the lungs of antigen sensitized animals. Again, treatment with insulin increased the number of eosinophils in the antigen sensitized diabetic animals. Experimental diabetes causes were found to decrease the airway reactivity and inflammatory responsiveness induced by antigen sensitization due to a reduction in the insulin levels.