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Peer-reviewedCC BY 4.0Gut Microbes

Disease-specific gut microbiota–metabolite–immune networks in hematologic disorders: mechanisms, causal support, and translational strategies

  • Li Yi1
  • Yuru Yuan2
  • Xiaolong Ma3
  • Chenxi Li4
  • Yushuo Hao5
  • Qianran Ma2
  • Xuexue Liu1
  • Xiao Du3,6
  • Lihua Shao3
  • Siliang Wang1,6
  • Jingyan Xu1,7
7 affiliations
  1. 1Department of Hematology, Nanjing Drum Tower Hospital Clinical College of Nanjing University of Chinese Medicine, Nanjing, China
  2. 2School of Life Sciences, Nanjing Normal University, Nanjing, China
  3. 3Department of Colorectal Surgery, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China
  4. 4Department of Pharmacy, Nanjing Drum Tower Hospital Clinical College of Nanjing University of Chinese Medicine, Nanjing, China
  5. 5Department of Thyroid, Metabolic and Hernia Surgery, The First Affiliated Hospital of Dalian Medical University, Dalian, China
  6. 6Department of Pharmacy, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China
  7. 7Department of Hematology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China
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Abstract

The gut microbiota is increasingly recognized as a systemic regulator of host immunity, host metabolism, epithelial barrier integrity, and distal tissue homeostasis. Hematologic disorders provide an important setting in which these host–microbe interactions converge on immune remodeling, marrow-niche function, hematopoietic recovery, treatment response, and transplant-related complications. This narrative review synthesizes mechanistic, clinical, and translational evidence linking gut microbial dysbiosis to benign and malignant hematologic diseases, clonal and premalignant states, and hematopoietic stem cell transplantation (HSCT)-related outcomes. Rather than treating microbiome associations as a single evidence category, we distinguish five complementary evidence strata: Mendelian randomization, experimental models, prospective human cohorts, randomized human interventions, and cross-sectional studies. These study designs address different causal questions and are interpreted as complementary rather than as a single linear hierarchy. We also separate microbial composition from microbial function: taxon-level enrichment or depletion is treated primarily as context-dependent and hypothesis-generating, whereas conserved functional pathways—including short-chain fatty acids, bile-acid transformation, tryptophan metabolism, microbial translocation and barrier dysfunction, and innate immune activation—provide the principal cross-disease mechanistic framework. We integrate disease-specific microbial features, functional mediators, immune and marrow consequences, and clinical outcomes into an author-constructed evidence map, while explicitly addressing bidirectionality, reverse causality, and translational readiness. Emerging applications include microbiota-based biomarkers, treatment-response prediction, fecal microbiota transplantation, probiotics and postbiotics, antibiotic stewardship, and microbiota-dependent modulation of drug metabolism.

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Cite

BibTeXRIS
BibTeX
@article{yi2026diseasespecific,
  title = {{Disease-specific gut microbiota–metabolite–immune networks in hematologic disorders: mechanisms, causal support, and translational strategies}},
  author = {Li Yi and Yuru Yuan and Xiaolong Ma and Chenxi Li and Yushuo Hao and Qianran Ma and Xuexue Liu and Xiao Du and Lihua Shao and Siliang Wang and Jingyan Xu},
  journal = {Gut Microbes},
  year = {2026},
  month = oct,
  doi = {10.1080/19490976.2026.2752469},
  url = {https://doi.org/10.1080/19490976.2026.2752469},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Disease-specific gut microbiota–metabolite–immune networks in hematologic disorders: mechanisms, causal support, and translational strategies
AU  - Li Yi
AU  - Yuru Yuan
AU  - Xiaolong Ma
AU  - Chenxi Li
AU  - Yushuo Hao
AU  - Qianran Ma
AU  - Xuexue Liu
AU  - Xiao Du
AU  - Lihua Shao
AU  - Siliang Wang
AU  - Jingyan Xu
PY  - 2026
DA  - 2026/10/29
JO  - Gut Microbes
DO  - 10.1080/19490976.2026.2752469
UR  - https://doi.org/10.1080/19490976.2026.2752469
AB  - The gut microbiota is increasingly recognized as a systemic regulator of host immunity, host metabolism, epithelial barrier integrity, and distal tissue homeostasis. Hematologic disorders provide an important setting in which these host–microbe interactions converge on immune remodeling, marrow-niche function, hematopoietic recovery, treatment response, and transplant-related complications. This narrative review synthesizes mechanistic, clinical, and translational evidence linking gut microbial dysbiosis to benign and malignant hematologic diseases, clonal and premalignant states, and hematopoietic stem cell transplantation (HSCT)-related outcomes. Rather than treating microbiome associations as a single evidence category, we distinguish five complementary evidence strata: Mendelian randomization, experimental models, prospective human cohorts, randomized human interventions, and cross-sectional studies. These study designs address different causal questions and are interpreted as complementary rather than as a single linear hierarchy. We also separate microbial composition from microbial function: taxon-level enrichment or depletion is treated primarily as context-dependent and hypothesis-generating, whereas conserved functional pathways—including short-chain fatty acids, bile-acid transformation, tryptophan metabolism, microbial translocation and barrier dysfunction, and innate immune activation—provide the principal cross-disease mechanistic framework. We integrate disease-specific microbial features, functional mediators, immune and marrow consequences, and clinical outcomes into an author-constructed evidence map, while explicitly addressing bidirectionality, reverse causality, and translational readiness. Emerging applications include microbiota-based biomarkers, treatment-response prediction, fecal microbiota transplantation, probiotics and postbiotics, antibiotic stewardship, and microbiota-dependent modulation of drug metabolism.
SN  - 1949-0976
SN  - 1949-0984
ER  -