Depressed immunological defence mechanisms in mice with experimentally induced diabetes

Abstract

Persistent diabetes mellitus with marked hyperglycemia was induced in mice by the administration of streptozotocin. In these streptozotocin-induced diabetic mice, resistance to tubercle bacillus challenge and primary as well as secondardy humoral immune responses against foreign erythrocytes were markedly depressed. The T-cell function in delayed hypersensitivity to 2,4-dinitro-1-fluorobenzene and bacterial phagocytic activity or peritoneal macrophages were markedly depressed. In contrast, the B-cell function in antibody production against T-independent antigen and the intracellular killing of bacteria in peritoneal macrophages were intact. We concluded that depression of the T-cell function or the phagocytic activity of macrophages or both may be the main immunological defect in these mice.

Lower expression of Th1-related cytokines and inducible nitric oxide synthase in mice with streptozotocin-induced diabetes mellitus infected withMycobacterium tuberculosis

“…This reduced expression correlated well with the impaired host resistance to this infection. In an earlier study, Saiki et al [6] demonstrated that diabetic mice established by administration of STZ exhibited weaker delayed-type hypersensitivity to PPD and were more prone to M. tuberculosis infection than control nondiabetic mice. However, these findings were not followed-up to define the mechanism.…”

Mycobacterial antigen-induced T helper type 1 (Th1) and Th2 reactivity of peripheral blood mononuclear cells from diabetic and non-diabetic tuberculosis patients andMycobacterium bovisbacilli Calmette–Guérin (BCG)-vaccinated healthy subjects

“…These immunological parameters became normal following successful therapies [9]. In addition, macrophage functions including bacterial phagocytic capacity, resistance to tubercle bacilli and T cell function in delayed type hypersensitivity, were also depressed in mice with experimentally induced diabetes [10]. These studies suggest that the functions of both T cells and macrophages are compromised in diabetes.…”

Bacterial Translocation from the Gastrointestinal Tract in Various Mouse Models for Human Diabetes

“…Streptozotocin may strongly depress the host immune systems for bacterial translocation. However, Saiki et al (12) reported that T-cell function and phagocytic activity in macrophages were depressed in streptozotocin-induced diabetic mice, both of which may reflect metabolic disturbance rather than direct toxic effects of streptozotocin to the host. Suppressed cell-mediated immunity in streptozotocin-incluced diabetes reverts to normal with insulin therapy (9).…”