Immunological and biochemical mechanisms of tuberculosis susceptibility in diabetes mellitus
Abdullaev R.Yu.1, Komissarova O.G.1,2, Mikhailovsky A.M.3
1 Central Research Institute of Tuberculosis, Moscow
2 Russian National Research Medical University named after N.I. Pirogov, Moscow.
3 Orenburg State Medical University
The problem of tuberculosis in patients with diabetes mellitus (DM) has been receiving increasing attention in recent years. The growing interest is due, on the one hand, to an increase in the number of patients with multidrug-resistant tuberculosis, and on the other, a steady increase in the prevalence of diabetes. Objective reality determines the urgency of the problem of the combined pathology, as well as the need for a proper understanding of the mechanisms of development of the tuberculous process in this category of patients.
The review covers literature data on the immunological and biochemical mechanisms of susceptibility to tuberculosis in diabetes mellitus. Analysis of the results of numerous studies suggests that the presence of diabetes is associated with a delayed immune response when infected with Mycobacterium tuberculosis (MTB). Hyperglycemia causes a disturbance in the function of macrophages, lymphocytes and neutrophils. In particular, the chemotactic and phagocytic function of macrophages decreases, the expression of signals from infected macrophages is blocked, the rate of migration of lymphocytes and neutrophils decreases, as well as the level of cytokines associated with congenital and acquired immunity. The combination of all these processes during the first 2 weeks after infection creates conditions for rapid multiplication of the MTB and thereby increases the risk of tuberculosis.
Key words: tuberculosis, diabetes mellitus, susceptibility, macrophages, neutrophils, lymphocytes, reactive oxygen intermediates.
For citation: Abdullaev R.Yu., Komissarova O.G., Mikhailovsky A.M. Immunological and biochemical mechanisms of tuberculosis susceptibility in diabetes mellitus // RMJ. 2017. № 18. P. 1324–1327.

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