Chemotherapy Alters Gut Microbiota To Limit Metastasis
Researchers found chemotherapy reshaped gut microbes, sending signals that unexpectedly helped block cancer spread.
In Nature Communications, researchers reveal that chemotherapy alters gut microbes and bone marrow immune cell development, unexpectedly reprogramming systemic immunity in ways that help restrict metastatic progression.
Research by Ludivine Bersier and directed by Tatiana Petrova, reported in Nature Communications reveals an unexpected systemic effect of chemotherapy that extends beyond its direct action on cancer cells.
Chemotherapy does not only kill tumor cells; it also damages the intestinal lining, causing well-known side effects. The researchers show that this gut injury changes nutrient availability for intestinal bacteria, reshaping the microbiota. As a result, certain bacteria increase the production of indole-3-propionic acid (IPA), a metabolite derived from tryptophan.
IPA acts as a long-distance signal, traveling from the gut to the bone marrow, where it reprograms immune cell production. It reduces the production of monocytes that suppress immunity and help cancer cells evade detection.
This immune shift strengthens T-cell activity and reorganizes immune interactions at metastatic sites, making the body less permissive to cancer spread, particularly to the liver. Importantly, patient data, investigated in close collaboration with Dr. Thibaud Koessler (HUG) support these findings: higher IPA levels following chemotherapy are associated with fewer monocytes and improved survival.
Together, these findings reveal a previously underappreciated gut–bone marrow–liver metastasis axis through which chemotherapy can exert durable systemic effects, opening new avenues to harness microbiota-derived metabolites as adjuvant strategies to limit metastasis.
Reference: Bersier L, Lorenzo-Martin LF, Chiang YH, et al. Chemotherapy-driven intestinal dysbiosis and indole-3-propionic acid rewire myelopoiesis to promote a metastasis-refractory state. Nat Commun. 2025. doi: 10.1038/s41467-025-67169-7
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