Microbial, Metabolic, and Inflammatory Features Associated with Delayed Diabetic Wound Healing in Mice
- 1Shandong University of Traditional Chinese Medicine, Jinan, Shandong Province, People’s Republic of China
- 2Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong Province, People’s Republic of China
Abstract
Introduction: Diabetic ulcers are characterized by delayed tissue repair, persistent inflammation, and wound microenvironment remodeling, yet the systemic and local molecular features associated with impaired diabetic wound healing remain incompletely defined.
Methods: In this exploratory pilot study, we profiled gut microbiota (16S rRNA sequencing), wound-tissue metabolites (liquid chromatography-mass spectrometry, LC-MS), and local gene expression (reverse transcription-quantitative polymerase chain reaction, RT-qPCR) in a mouse model of diabetic ulcers. Three biological replicates per group (n = 3 mice/group) were included in each analytical platform.
Results: Compared with non-diabetic wound controls, diabetic mice showed delayed healing alongside altered gut microbial structures, including enrichment of Clostridiales and Mucispirillum and depletion of Lactobacillus. Wound metabolomics tentatively identified candidate metabolic shifts involving molecules such as 16-oxopalmitate and indoleacetaldehyde. Locally, candidate pro-inflammatory genes (Il1b, Tnf, Nos2, Mmp9) were upregulated, whereas candidate repair-associated markers (Arg1, Vegfa) were decreased. Correlation analysis further connected selected diabetes-associated microbial changes with local wound metabolic remodeling, revealing exploratory associations among gut microbial features, wound metabolites, and local inflammatory/repair-related gene expression in delayed diabetic wound healing.
Discussion: In view of very small sample size (n = 3 per group), these findings provide hypothesis-generating preclinical evidence relevant to diabetic wound microenvironment remodeling, and indicates specific microbial, metabolic, and gene-expression targets for larger validation studies.
Related
- Computed Tomographic Features Associated with Pulmonary Melioidosis versus Pulmonary Tuberculosis in Diabetic Patients: A Retrospective Comparative Cohort Study.
- Computer-aided diagnosis of metabolic dysfunction-associated steatotic liver disease using paired liver–kidney texture features
- Network Pharmacology-Assisted Multi-Omics Analysis of Gut Microbiota-Host Metabolic Remodeling and Hepatic HPD/GSTM3-Associated Redox Responses Following Shanqijing Treatment in STZ-Induced Diabetic Mice.
- Entresto attenuates dexamethasone-induced metabolic dysfunction-associated steatotic features in rats: role of potential SGK1/FOXO3a regulatory pathway and cardio-metabolic axis
- METABOLIC DYSFUNCTION-ASSOCIATED STEATOTIC LIVER DISEASE IN PATIENTS WITH INFLAMMATORY BOWEL DISEASE: ASSOCIATION WITH BODY MASS INDEX AND DISEASE SEVERITY
BibTeX
@article{wei2026microbial,
title = {{Microbial, Metabolic, and Inflammatory Features Associated with Delayed Diabetic Wound Healing in Mice}},
author = {Jian Liang Wei and Ya Nan Zhao and Ming Liu},
journal = {Clinical, Cosmetic and Investigational Dermatology},
year = {2026},
month = oct,
doi = {10.2147/ccid.s640155},
url = {https://doi.org/10.2147/ccid.s640155},
note = {CC BY-NC 4.0},
}
RIS
TY - JOUR
TI - Microbial, Metabolic, and Inflammatory Features Associated with Delayed Diabetic Wound Healing in Mice
AU - Jian Liang Wei
AU - Ya Nan Zhao
AU - Ming Liu
PY - 2026
DA - 2026/10/30
JO - Clinical, Cosmetic and Investigational Dermatology
DO - 10.2147/ccid.s640155
UR - https://doi.org/10.2147/ccid.s640155
AB - Introduction: Diabetic ulcers are characterized by delayed tissue repair, persistent inflammation, and wound microenvironment remodeling, yet the systemic and local molecular features associated with impaired diabetic wound healing remain incompletely defined. Methods: In this exploratory pilot study, we profiled gut microbiota (16S rRNA sequencing), wound-tissue metabolites (liquid chromatography-mass spectrometry, LC-MS), and local gene expression (reverse transcription-quantitative polymerase chain reaction, RT-qPCR) in a mouse model of diabetic ulcers. Three biological replicates per group (n = 3 mice/group) were included in each analytical platform. Results: Compared with non-diabetic wound controls, diabetic mice showed delayed healing alongside altered gut microbial structures, including enrichment of Clostridiales and Mucispirillum and depletion of Lactobacillus. Wound metabolomics tentatively identified candidate metabolic shifts involving molecules such as 16-oxopalmitate and indoleacetaldehyde. Locally, candidate pro-inflammatory genes (Il1b, Tnf, Nos2, Mmp9) were upregulated, whereas candidate repair-associated markers (Arg1, Vegfa) were decreased. Correlation analysis further connected selected diabetes-associated microbial changes with local wound metabolic remodeling, revealing exploratory associations among gut microbial features, wound metabolites, and local inflammatory/repair-related gene expression in delayed diabetic wound healing. Discussion: In view of very small sample size (n = 3 per group), these findings provide hypothesis-generating preclinical evidence relevant to diabetic wound microenvironment remodeling, and indicates specific microbial, metabolic, and gene-expression targets for larger validation studies.
SN - 1178-7015
ER -