ArticleJournal of translational medicine2026
Immuno-metabolic dysregulation in type 2 diabetes is associated with altered neutrophil functional plasticity, mitochondrial dysfunction, and compromised responses in sepsis.
Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Identification of immune cell mitochondrial dysfunction characteristics and clinical predictive biomarkers in sepsis via multi-cohort machine learning and single-cell RNA sequencing.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Article
- Neutrophil extracellular traps in asthma and chronic obstructive pulmonary disease: pathogenic roles, and therapeutic opportunities.Frontiers in immunology · 2026Review
- Mitochondrial reprogramming of neutrophil extracellular traps in chronic obstructive pulmonary disease and asthma: toward a phenotype-driven therapeutic framework.Frontiers in immunology · 2026Review
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Authors and funding
13 authors.
Funding
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Abstract
backgroundConstitutively activated neutrophil extracellular traps (NETs) have been implicated in the impeded response to infections in Type 2 Diabetes (T2D). However, immuno-metabolic factors contributing to functional plasticity of neutrophils in T2D associated infections are not known.
methodsUsing both human and mice model of sepsis with either diabetic or non-diabetic background, we investigated functionally confined neutrophil subpopulations either executing phagocytosis or NETosis. An integrated analysis of cytokines regulating granulopoiesis, RNAseq of NETs forming neutrophils and metabolomics was performed. Mitochondrial function was assessed via measuring mitochondrial membrane potential, cellular oxygen consumption rate and mitophagy.
resultsWe identified neutrophil subpopulations either executing phagocytosis or NETosis. Proportions of these functionally restricted neutrophils are significantly altered in T2D and fail to elicit an immune response upon induction of sepsis. Integrated analysis involving cytokines, transcriptome and metabolome data revealed perturbed immunometabolic axis in T2D models majorly effecting mitochondrial metabolism. Molecular dynamic simulations indicate deformed lipid densities and disrupted inner mitochondrial membrane. T2D neutrophils showed decrease in mitochondrial membrane potential, cellular oxygen consumption rate and mitophagy. Arachidonic acid supplementation activated mitochondrial ROS and restored NETs formation in T2D upon sepsis.
conclusionsIn mouse models, along with preliminary findings in human subjects, our study provides novel and correlative insights into the relationship between metabolic changes and neutrophil dysfunction in T2D-associated sepsis, exploring immuno-metabolism as a therapeutic target to improve neutrophil function.
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