Mechanisms of Immune Inflammation Formation in Bro-Nchial Asthma, Combined with Metabolically Important States: Obesity or Diabetes Mellitus Type II

Aim: To conduct the study of the formation mechanisms of immune inflammation in patients with asthma, asthma-associated obesity, and asthma in association with type II diabetes mellitus (DM). Materials and methods: 155 patients who were divided into 3 groups - with BA - I group (32), asthma and obesity - II group (52), asthma and DM type II - III group (71) were examined. In all patients the parameters of cellular and humoral immunity phagocytic activity of neutrophils were studied. Results. In patients with asthma, asthma, asthma and obesity, asthma associated with type II DM indicates the formation of a deficiency in the cellular immunity, the severity of which was most significant in patients with asthma associated with type 2 DM. All patients had dysfunction of phagocytic cells, which was most significant in asthma associated with type II DM. In patients with asthma and asthma, combined with obesity, activation of nonspecific and specific components of the humoral immune response was noted. In patients with asthma associated with type 2 diabetes, the lack of specificity with a decrease in IgE is observed with the strain of nonspecific immunity. The increase in the level of lymphocytic antibodies in the blood of patients with asthma associated with obesity and asthma associated with type 2 diabetes, along with a decrease in the total number of circulated immune complexes (CIC), indicates the formation of an autoimmune component of inflammation in the comorbidity of asthma and obesity, and may adversely affect changes in cellular unit of immunity. Conclusions: The decrease in IgE level in patients with asthma associated with type II diabetes, along with an increase in the number of lymphocyte autoantibodies, indicates pathogenic changes in the combination of asthma with the most metabolically significant disease: a decrease in the severity of the allergic component of inflammation and its replacement by an autoimmune, which is more aggressive.