Reduced Th1 response is associated with lower glycolytic activity in activated peripheral blood mononuclear cells after metabolic and bariatric surgery

Villarreal-Calderón, José R; Castillo, Elena C.; Cuellar-Tamez, R X; García-Garza, Manuel; Elizondo‐Montemayor, Leticia; García‐Rivas, Gerardo

doi:10.1007/s40618-021-01587-4

Cited by 6 publications

(3 citation statements)

References 61 publications

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“…It is worth noting that inflammation is reported to be the main player linking obesity with its related metabolic perturbations [ 36 ] and is ameliorated after weight loss. A significant reduction in systemic cytokines—TNFɑ, IL6 and IL1β—and decreased MCP1 and NF-κB protein expression were detected in the leukocytes of our patients after RYGB, which is in line with previous reports of an overall reduction in inflammatory markers in leukocytes [ 37 ] and adipose tissue [ 23 ]. The complex inflammatory network that characterises obesity is mostly activated by an oxidative stress status.…”

Section: Discussionsupporting

confidence: 92%

Impact of Roux-en-Y Gastric Bypass on Mitochondrial Biogenesis and Dynamics in Leukocytes of Obese Women

et al. 2022

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The chronic low-grade inflammation widely associated with obesity can lead to a prooxidant status that triggers mitochondrial dysfunction. To date, Roux-en-Y gastric bypass (RYGB) is considered the most effective strategy for obese patients. However, little is known about its molecular mechanisms. This interventional study aimed to investigate whether RYGB modulates oxidative stress, inflammation and mitochondrial dynamics in the leukocytes of 47 obese women at one year follow-up. We evaluated biochemical parameters and serum inflammatory cytokines -TNFα, IL6 and IL1β- to assess systemic status. Total superoxide production -dHe-, mitochondrial membrane potential -TMRM-, leucocyte protein expression of inflammation mediators -MCP1 and NF-kB-, antioxidant defence -GPX1-, mitochondrial regulation—PGC1α, TFAM, OXPHOS and MIEAP- and dynamics -MFN2, MNF1, OPA1, FIS1 and p-DRP1- were also determined. After RYGB, a significant reduction in superoxide and mitochondrial membrane potential was evident, while GPX1 content was significantly increased. Likewise, a marked upregulation of the transcription factors PGC1α and TFAM, complexes of the oxidative phosphorylation chain (I–V) and MIEAP and MFN1 was observed. We conclude that women undergoing RYGB benefit from an amelioration of their prooxidant and inflammatory status and an improvement in mitochondrial dynamics of their leukocytes, which is likely to have a positive effect on clinical outcome.

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Section: Discussionsupporting

confidence: 92%

Impact of Roux-en-Y Gastric Bypass on Mitochondrial Biogenesis and Dynamics in Leukocytes of Obese Women

et al. 2022

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“…As Th1 cells depend on glycolysis, AMPK activator metformin suppresses the differentiation of Th1 and Th17 cells while promoting Treg cells in nonobese diabetic mice model (Duan et al, 2019). Metabolic and bariatric surgery (MBS) reduces the production of IFN-γ and Th1 cell population which is higher in obese people, suggesting that MBS minimizes the glycolytic activity of Th1 cells (Villarreal-Calderón et al, 2021). Lactate dehydrogenase (LDHA) which is upregulated during glycolysis plays an important role in Th1 differentiation and function.…”

Section: Th1 Cellsmentioning

confidence: 99%

Regulation of immune cell metabolism in health and disease: Special focus on T and B cell subsets

Chakraborty

Khamaru

Bhattacharyya

2022

Cell Biology International

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Metabolism is a dynamic process and keeps changing from time to time according to the demand of a particular cell to meet its bio‐energetic requirement. Different immune cells rely on distinct metabolic programs which allow the cell to balance its requirements for energy, molecular biosynthesis, and effector activity. In the aspect of infection and cancer immunology, effector T and B cells get exhausted and help tumor cells to evade immunosurveillance. On the other hand, T cells become hyperresponsive in the scenario of autoimmune diseases. In this article, we have explored the uniqueness and distinct metabolic features of key CD4+ T and B helper cell subsets, CD4+ T, B regulatory cell subsets and CD8+ T cells regarding health and disease. Th1 cells rely on glycolysis and glutaminolysis; inhibition of these metabolic pathways promotes Th1 cells in Treg population. However, Th2 cells are also dependent on glycolysis but an abundance of lactate within TME shifts their metabolic dependency to fatty acid metabolism. Th17 cells depend on HIF‐1α mediated glycolysis, ablation of HIF‐1α reduces Th17 cells but enhance Treg population. In contrast to effector T cells which are largely dependent on glycolysis for their differentiation and function, Treg cells mainly rely on FAO for their function. Therefore, it is of utmost importance to understand the metabolic fates of immune cells and how it facilitates their differentiation and function for different disease models. Targeting metabolic pathways to restore the functionality of immune cells in diseased conditions can lead to potent therapeutic measures.

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“…In this term, metabolic and neuroendocrine responses are triggered to maintain metabolic energy and the activated immune system [ 1 ]. The inflammatory environment induces the activation of T cells, CD8+ cytotoxic T lymphocytes (CTLs), and CD4+ helper T cells (Th), triggering their proliferation and differentiation into effector T cells [ 2 ]. The production of cytokines such as interferon-gamma (IFN-γ) and interleukin (IL)-17 by the Th cells contributes to the proinflammatory state, activating macrophages and B cells, leading to systemic inflammation [ 3 ].…”

Section: Introduction: Cellular and Molecular Mechanisms Of Brain And...mentioning

confidence: 99%

Central and Peripheral Inflammation: A Common Factor Causing Addictive and Neurological Disorders and Aging-Related Pathologies

Escobar,

Bonansco,

Cruz

et al. 2023

IJMS

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Many diseases and degenerative processes affecting the nervous system and peripheral organs trigger the activation of inflammatory cascades. Inflammation can be triggered by different environmental conditions or risk factors, including drug and food addiction, stress, and aging, among others. Several pieces of evidence show that the modern lifestyle and, more recently, the confinement associated with the COVID-19 pandemic have contributed to increasing the incidence of addictive and neuropsychiatric disorders, plus cardiometabolic diseases. Here, we gather evidence on how some of these risk factors are implicated in activating central and peripheral inflammation contributing to some neuropathologies and behaviors associated with poor health. We discuss the current understanding of the cellular and molecular mechanisms involved in the generation of inflammation and how these processes occur in different cells and tissues to promote ill health and diseases. Concomitantly, we discuss how some pathology-associated and addictive behaviors contribute to worsening these inflammation mechanisms, leading to a vicious cycle that promotes disease progression. Finally, we list some drugs targeting inflammation-related pathways that may have beneficial effects on the pathological processes associated with addictive, mental, and cardiometabolic illnesses.

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Reduced Th1 response is associated with lower glycolytic activity in activated peripheral blood mononuclear cells after metabolic and bariatric surgery

Cited by 6 publications

References 61 publications

Impact of Roux-en-Y Gastric Bypass on Mitochondrial Biogenesis and Dynamics in Leukocytes of Obese Women

Impact of Roux-en-Y Gastric Bypass on Mitochondrial Biogenesis and Dynamics in Leukocytes of Obese Women

Regulation of immune cell metabolism in health and disease: Special focus on T and B cell subsets

Central and Peripheral Inflammation: A Common Factor Causing Addictive and Neurological Disorders and Aging-Related Pathologies

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