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Microbiome modulation uncouples efficacy and toxicity induced by immune checkpoint blockade in mouse multiple myeloma

Laura Lucia Cogrossi1,2, Anna Policastro1, Paola Zordan1

  • 1Cellular immunology Unit, Division of Immunology, Transplantation and Infectious Diseases, IRCCS Ospedale San Raffaele, Milan, Italy.

Nature Communications
|November 25, 2025
PubMed

Insights

Gut bacteria Prevotella melaninogenica and its metabolite butyrate delay multiple myeloma progression. This approach may offer new treatments for plasma cell disorders by modulating gut microbiota and short-chain fatty acids.

Area of Science:

  • Immunology
  • Microbiology
  • Oncology

Background:

  • Smoldering multiple myeloma (SMM) can progress to life-threatening multiple myeloma (MM).
  • Intestinal microbiota and T helper-17 (Th17) cells are implicated in MM development, but mechanisms remain unclear.
  • Understanding these mechanisms is crucial for developing effective therapies.

Purpose of the Study:

  • To investigate the role of Prevotella melaninogenica in the progression of SMM to MM.
  • To elucidate the mechanisms by which gut microbiota influences myeloma development.
  • To explore potential therapeutic strategies targeting gut microbiota and its metabolites.

Main Methods:

  • Administration of Prevotella melaninogenica to transgenic mice with SMM-like phenotypes.
  • Analysis of short-chain fatty acid (SCFA) production.
  • Flow cytometry to assess dendritic cell and Th17 cell phenotypes.
  • Evaluation of synergistic effects with immunotherapy (anti-PD-L1, anti-TIGIT).
  • Assessment of IL-17-mediated skin lesions.

Main Results:

  • P. melaninogenica administration delayed the progression from SMM to MM in mice.
  • P. melaninogenica increased SCFA production, preventing a pro-Th17 cell phenotype in dendritic cells.
  • Reduced Th17 cell accumulation in the bone marrow of treated mice.
  • P. melaninogenica and butyrate synergized with immunotherapies to suppress myeloma by modulating T cell responses.
  • P. melaninogenica attenuated IL-17-mediated skin lesions.

Conclusions:

  • Gut microbiota modulation, specifically with P. melaninogenica, can delay multiple myeloma progression.
  • SCFA administration may prevent Th17 cell-driven myeloma development.
  • Combined strategies involving gut microbiota, SCFAs, and immunotherapy show promise for treating plasma cell dyscrasias.

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