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Role of Oxidative Stress in Tuberculosis Meningitis Infection in Diabetics
Inesa Navasardyan1, Stephanie Yeganyan1, Helena Nguyen1
1College of Osteopathic Medicine of the Pacific, Western University of Health Sciences, Pomona, CA 91766, USA.
Abstract:
Tuberculosis meningitis (TBM) is a result of the invasion of the meninges with the bacilli of Mycobacterium tuberculosis (Mtb), leading to inflammation of the meninges around the brain or spinal cord. Oxidative stress occurs when the body's cells become overwhelmed with free radicals, particularly reactive oxygen species (ROS). ROS plays a significant role in the pathogenesis of TBM due to their toxic nature, resulting in impairment of the body's ability to fight off infection. ROS damages the endothelial cells and impairs the defense mechanisms of the blood-brain barrier (BBB), which contributes to CNS susceptibility to the bacteria causing TBM. Diabetes mellitus (DM) is a common condition that is characterized by the impairment of the hormone insulin, which is responsible for modulating blood glucose levels. The increased availability of glucose in individuals with diabetes results in increased cellular activity and metabolism, leading to heightened ROS production and, in turn, increased susceptibility to TBM. In this review, we summarize our current understanding of oxidative stress and its role in both TBM and DM. We further discuss how increased oxidative stress in DM can contribute to the likelihood of developing TBM and potential therapeutic approaches that may be of therapeutic value.
Insights
Tuberculosis meningitis (TBM) involves oxidative stress, where reactive oxygen species (ROS) damage the brain and blood-brain barrier. Diabetes mellitus exacerbates this, increasing TBM risk and highlighting the need for new therapies.
Area of Science:
- Neuroscience
- Immunology
- Endocrinology
Background:
- Tuberculosis meningitis (TBM) arises from Mycobacterium tuberculosis invasion, causing inflammation around the brain and spinal cord.
- Oxidative stress, an imbalance of reactive oxygen species (ROS), significantly contributes to TBM pathogenesis.
- Diabetes mellitus (DM) involves impaired insulin function, leading to hyperglycemia and increased ROS production.
Purpose of the Study:
- To review the role of oxidative stress in TBM and DM.
- To explore how DM-associated oxidative stress increases TBM susceptibility.
- To discuss potential therapeutic strategies for TBM and DM.
Main Methods:
- Literature review of studies on TBM, DM, and oxidative stress.
- Analysis of the mechanisms linking ROS to TBM pathogenesis.
- Examination of the impact of hyperglycemia on ROS production in DM.
Main Results:
- ROS damages endothelial cells and compromises the blood-brain barrier (BBB), increasing CNS susceptibility to Mtb.
- Increased cellular metabolism in DM leads to heightened ROS production, elevating TBM risk.
- Oxidative stress is a critical factor in the interplay between DM and TBM.
Conclusions:
- Oxidative stress plays a central role in the pathogenesis of both TBM and DM.
- DM-induced oxidative stress significantly increases the risk of developing TBM.
- Targeting oxidative stress pathways may offer promising therapeutic avenues for TBM and DM.
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