Immunopathology of metabolic syndrome: effects on gut microbiota and antibiotic resistance
6 affiliations
- 1Department of Bacteriology, Pasteur Institute of Iran
- 2Division of Microbiology, Department of Pathobiology, School of Public Health, Tehran University of Medical Sciences
- 3Faculty of Medicine, University of Bergen
- 4Department of Microbiology, Danylo Halytsky Lviv National Medical University
- 5Oslo Bioconsulting
- 6School of Medicine, Shahroud University of Medical Sciences
Abstract
The cluster of related metabolically derived disorders that confer increased risk of developing type 2 diabetes mellitus (T2D) and cardiovascular disease (CVD) is termed the Metabolic syndrome (MetS). Despite two decades of growing evidence on MetS pathogenesis, the immunopathological links between gut microbiota (GM) dysbiosis and metabolic derangements remain only partially elucidated. This review focuses on the complex nexus among MetS, GM composition and function, and the emerging antibiotic-resistance predicament. The gut commensal microbiome-defined as approximately 10 ¹⁴ microorganisms that have been termed endocrine organs with key roles beyond gastrointestinal homeostasis, such as immune-mediated host inflammatory and metabolic regulation and barrier homeostasis- undergoes dysbiosis in MetS, characterized by marked losses of beneficial short-chain fatty acid (SCFA)-producing bacteria and overgrowth of pathobiont Proteobacteria , such as those bearing lipopolysaccharide. Increased gut permeability and Toll-like receptor 4 (TLR-4) activation, driven by increased luminal products, are termed metabolic endotoxemia and form the immunopathological bridge between gut dysbiosis and systemic low-grade inflammation and insulin resistance. Disturbances in microbial-mediated host metabolism of bile acids, tryptophan catabolism, and the regulatory T cell/T helper 17 axis further promote inflammation in adipose tissue, liver, and skeletal muscle. Antibiotic-driven dysbiosis, which reduces diversity and increases antibiotic-resistant gene elements within the host gut resistome, exacerbates metabolic abnormalities and is a key focus for developing personalized treatment approaches.
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BibTeX
@article{namadian2026immunopathology,
title = {{Immunopathology of metabolic syndrome: effects on gut microbiota and antibiotic resistance}},
author = {Navid Namadian and Valentyn Oksenych and Zahra Asadi and Niloofar Kiaheyrati and Hamed Tahmasebi},
journal = {Frontiers in Immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.1926461},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1926461/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Immunopathology of metabolic syndrome: effects on gut microbiota and antibiotic resistance
AU - Navid Namadian
AU - Valentyn Oksenych
AU - Zahra Asadi
AU - Niloofar Kiaheyrati
AU - Hamed Tahmasebi
PY - 2026
DA - 2026/10/30
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1926461
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1926461/full
AB - The cluster of related metabolically derived disorders that confer increased risk of developing type 2 diabetes mellitus (T2D) and cardiovascular disease (CVD) is termed the Metabolic syndrome (MetS). Despite two decades of growing evidence on MetS pathogenesis, the immunopathological links between gut microbiota (GM) dysbiosis and metabolic derangements remain only partially elucidated. This review focuses on the complex nexus among MetS, GM composition and function, and the emerging antibiotic-resistance predicament. The gut commensal microbiome-defined as approximately 10 ¹⁴ microorganisms that have been termed endocrine organs with key roles beyond gastrointestinal homeostasis, such as immune-mediated host inflammatory and metabolic regulation and barrier homeostasis- undergoes dysbiosis in MetS, characterized by marked losses of beneficial short-chain fatty acid (SCFA)-producing bacteria and overgrowth of pathobiont Proteobacteria , such as those bearing lipopolysaccharide. Increased gut permeability and Toll-like receptor 4 (TLR-4) activation, driven by increased luminal products, are termed metabolic endotoxemia and form the immunopathological bridge between gut dysbiosis and systemic low-grade inflammation and insulin resistance. Disturbances in microbial-mediated host metabolism of bile acids, tryptophan catabolism, and the regulatory T cell/T helper 17 axis further promote inflammation in adipose tissue, liver, and skeletal muscle. Antibiotic-driven dysbiosis, which reduces diversity and increases antibiotic-resistant gene elements within the host gut resistome, exacerbates metabolic abnormalities and is a key focus for developing personalized treatment approaches.
SN - 1664-3224
ER -