Steve Ferlita, Aram Yegiazaryan, Navid Noori, Gagandeep Lal, Timothy Nguyen, Kimberly To, Vishwanath Venketaraman
Journal: Journal of clinical medicine 2019;8(12):2219
PMID: 31888124
Uncontrolled type 2 diabetes can alter the immune system and increase the risk of infections such as Mycobaterium tuberculosis (M. tb). Understanding how this can occur and the possible strategies to enhance the immune system is critical to prevent co-infections. This review of 69 papers aimed to discuss how concurrent infections can be prevented. The paper starts by discussing the ways that type 2 diabetes can alter the immune response, such as persistent high blood sugar levels leading to the production of harmful chemicals when protein or fat combine with sugar in the bloodstream and increased inflammation. Complex pathways are triggered by these two events resulting in an altered immune response. In particular glutathione, an antioxidant is decreased, which is important in the immune response when controlling M. tb. It was concluded that high blood sugar can increase inflammation and decrease glutathione resulting in immune suppression. This paper could be used by health care professionals to understand the complex mechanisms whereby type 2 diabetes can suppress the immune system resulting in a high risk of infections.
There has been an alarming increase in the incidence of Type 2 Diabetes Mellitus (T2DM) worldwide. Uncontrolled T2DM can lead to alterations in the immune system, increasing the risk of susceptibility to infections such as . Altered immune responses could be attributed to factors such as the elevated glucose concentration, leading to the production of Advanced Glycation End products (AGE) and the constant inflammation, associated with T2DM. This production of AGE leads to the generation of reactive oxygen species (ROS), the use of the reduced form of nicotinamide adenine dinucleotide phosphate (NADPH) via the Polyol pathway, and overall diminished levels of glutathione (GSH) and GSH-producing enzymes in T2DM patients, which alters the cytokine profile and changes the immune responses within these patients. Thus, an understanding of the intricate pathways responsible for the pathogenesis and complications in T2DM, and the development of strategies to enhance the immune system, are both urgently needed to prevent co-infections and co-morbidities in individuals with T2DM.
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