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Updated: Jan 31, 2026

Quantitative Polymerase Chain Reaction-based Analyses of Murine Intestinal Microbiota After Oral Antibiotic Treatment
Published on: November 17, 2018
The Gastro-Intestinal Microbiota in Haematology
José Manuel Moreno-Mirón1, Guillermo José Ruiz-Argüelles2, Moisés Manuel Gallardo-Pérez3
1Universidad Panamericana, Mexico City, Mexico.
Background:
The gastro-intestinal microbiota is a key regulator of systemic immunity and inflammatory tone and it contributes to normal haematopoiesis through microbial metabolites, barrier integrity, and host-microbe immune signalling. Disruption of this has been increasingly linked to the development, clinical course, and treatment-related complications of haematological disorders, including clonal haematopoiesis of indeterminate potential (CHIP), leukaemias, and plasma cell neoplasms (PCNs).
Summary:
This review synthesises current evidence on how gut microbiota composition and function intersect with haematopoietic regulation and haematological disease biology. We summarise proposed mechanisms - including microbe-derived metabolites (e.g., short-chain fatty acids), pattern-recognition receptor signalling, intestinal permeability, and cytokine-mediated inflammation - that may influence haematopoietic stem and progenitor cell behaviour and immune cell differentiation. We then discuss disease-specific associations of dysbiosis with CHIP, leukaemias, and PCN, as well as the impact of common haematology interventions (antibiotics, chemotherapy, immunomodulatory therapies, and transplantation) on microbial ecology and downstream clinical outcomes. Finally, we highlight methodological challenges and outline priorities for longitudinal, mechanistic, and multi-omics studies to enable microbiota-informed risk stratification and therapeutic modulation.
Key Messages:
(1) The gut microbiota influences haematopoiesis via immune signalling, microbial metabolites, and maintenance of mucosal barrier function. (2) Dysbiosis is associated with CHIP, leukaemias, and PCN, and may contribute through chronic inflammation and altered immune homeostasis. (3) Haematological therapies frequently reshape the microbiota; these changes may affect infection risk, treatment tolerance, and outcomes. (4) Current evidence is largely associative; rigorously designed longitudinal and interventional studies are needed to establish causality and guide clinical translation.
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