Frontiers in microbiology · 2026
MaaT013 fecal microbiotherapy modulates key gastro-intestinal and immunological processes involved in GvHD pathogenesis in vitro and in vivo.
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Laperrousaz Bastien, Reygner Julie, de Seilhac Margaux, Sabourin Antoine, Bompard Cassandra, Gasc Cyrielle, Prestat Emmanuel, Levast Benoît, Petitjean Charlotte, Declomesnil Sophie, Godefroy Emmanuelle, Schwintner Carole, Corvaïa Nathalie, Jenq Robert R, Holler Ernst
Аннотация
BACKGROUND: Acute graft-vs.-host disease (aGvHD) is a life-threatening complication of allogeneic hematopoietic cell transplantation (allo-HCT), where allogeneic donor T cells recognize recipient tissues as foreign and damage them. Gut microbiota disruption following allo-HCT has been associated with increased aGvHD incidence, severity, and mortality. Growing clinical evidence suggests the efficacy of fecal microbiotherapy to restore a healthy and diverse gut microbiota and to treat aGvHD. MaaT013 (Xervyteg®), a standardized allogeneic fecal microbiotherapy derived from pooled healthy human fecal microbiota, has demonstrated efficacy in mitigating steroid-refractory aGvHD in the Phase 2 HERACLES trial, and is currently being evaluated in the pivotal ARES trial in ruxolitinib-resistant aGvHD with gastrointestinal involvement.
METHODS: Here, multi-omics analyses across complementary in vitro and in vivo models suggest that MaaT013 modulates biological processes involved in aGvHD pathogenesis.
RESULTS: First, MaaT013-derived metabolites prevented inflammation-induced gut barrier alteration in an in vitro leaky gut model. Second, MaaT013 stimulated dendritic cell-mediated Tregs amplification and subsequent release of IL-10 and TGF-b in vitro. Third, beneficial bacteria from MaaT013 engrafted in the gut of germ-free mice, producing anti-inflammatory metabolites and restoring healthy gut physiology through immune rebalancing. Finally, MaaT013 delayed the appearance of aGvHD symptoms in a specific-pathogen free xenogeneic mouse model of aGvHD.
DISCUSSION: Together, these results provide exploratory, multi-model evidence of MaaT013's potential to mitigate aGvHD by restoring microbial diversity, gut integrity, and immune homeostasis.
METHODS: Here, multi-omics analyses across complementary in vitro and in vivo models suggest that MaaT013 modulates biological processes involved in aGvHD pathogenesis.
RESULTS: First, MaaT013-derived metabolites prevented inflammation-induced gut barrier alteration in an in vitro leaky gut model. Second, MaaT013 stimulated dendritic cell-mediated Tregs amplification and subsequent release of IL-10 and TGF-b in vitro. Third, beneficial bacteria from MaaT013 engrafted in the gut of germ-free mice, producing anti-inflammatory metabolites and restoring healthy gut physiology through immune rebalancing. Finally, MaaT013 delayed the appearance of aGvHD symptoms in a specific-pathogen free xenogeneic mouse model of aGvHD.
DISCUSSION: Together, these results provide exploratory, multi-model evidence of MaaT013's potential to mitigate aGvHD by restoring microbial diversity, gut integrity, and immune homeostasis.