Immune dysfunction in patients with diabetes mellitus (DM)

Abstract

Patients with diabetes mellitus (DM) have infections more often than those without DM. The course of the infections is also more complicated in this patient group. One of the possible causes of this increased prevalence of infections is defects in immunity. Besides some decreased cellular responses in vitro, no disturbances in adaptive immunity in diabetic patients have been described. Different disturbances (low complement factor 4, decreased cytokine response after stimulation) in humoral innate immunity have been described in diabetic patients. However, the clinical relevance of these findings is not clear. Concerning cellular innate immunity most studies show decreased functions (chemotaxis, phagocytosis, killing) of diabetic polymorphonuclear cells and diabetic monocytes/macrophages compared to cells of controls. In general, a better regulation of the DM leads to an improvement of these cellular functions. Furthermore, some microorganisms become more virulent in a high glucose environment. Another mechanism which can lead to the increased prevalence of infections in diabetic patients is an increased adherence of microorganisms to diabetic compared to nondiabetic cells. This has been described for Candida albicans. Possibly the carbohydrate composition of the receptor plays a role in this phenomenon.

Type 2 Diabetes Mellitus Coincident with Pulmonary Tuberculosis Is Associated with Heightened Systemic Type 1, Type 17, and Other Proinflammatory Cytokines

“…One possible mechanism is that an impaired immune response in diabetic patients facilitates either primary infection with tuberculosis or reactivation of latent tuberculosis (11). Studies examining the innate and adaptive immune response to microbial antigens in diabetic patients suggest that these responses are compromised, particularly in patients with chronic hyperglycemia (12)(13)(14). Whether this applies to tuberculosis infection remains unclear.…”

How does cytomegalovirus factor into diseases of aging and vaccine responses, and by what mechanisms?

“…This can be explained by the fact that the direct deleterious effects of CMVon pancreatic cells might have become significant after a long period of CMV infection. Moreover, hyperglycemia has been shown to impair host defenses and responses to infection, which may lead to higher seroprevalence of CMV in T2D patients (Geerlings and Hoepelman 1999). Thus, higher prevalence of CMV would be a result, not a cause, of disease.…”

Intensive glucose control after allogeneic hematopoietic stem cell transplantation: a retrospective matched-cohort study

“…The reduction in infectious diseases by IGC may reflect the deleterious effects of hyperglycemia on macrophage or neutrophil function or insulin-induced protective effects on mucosal and skin barriers. [24][25][26][27] The improvement of innate immunity could be quite important, especially during the period of granulocytopenia after allogeneic HSCT. The protection of mucosal tissues could reduce bacterial translocation, which might lead to a reduced incidence of sepsis.…”