Authors
Panida Sittipo, Joon-Young Park, Eunike Tiffany, Ara Oh, Subin Moon, Chan Hee Lee, Jae Sang Oh, Tae-Young Kim, Mi-Na Kweon, Jaeseoung Choi, Keon-Hyoung Song, Dong-Woo Lee, Myung Hee Nam, Soo-Jong Hong, Eun-Young Lee, Seong Ran Jeon, Ho-Yeon Song, Bong-Soo Kim, Yun Kyung Lee
Published in
Experimental & molecular medicine. Jul 14, 2026. Epub Jul 14, 2026.
Abstract
The progression of multiple sclerosis (MS) is potentially influenced by the microbiome. Elucidating host-microbiome interactions in MS may aid in developing microbiome-based applications; however, these interactions remain unclear. Here, we aimed to elucidate how Veillonella ratti MHL0042, isolated from human infant feces, modulates neuroinflammation and disease severity in experimental autoimmune encephalomyelitis, a murine MS model. Whole metagenomic sequencing revealed that V. ratti MHL0042 reshaped disrupted gut microbiota via microbial interactions throughout the intestinal tract. V. ratti MHL0042 administration significantly reduced central nervous system inflammation, notably decreasing CD4+IFN-γ⁺ T cell populations and activated spinal cord microglia. Mechanistically, V. ratti MHL0042 depleted pldA-containing bacteria, involved in phosphatidylethanolamine metabolism, thus elevating dioleoyl phosphatidylethanolamine (DOPE) levels. Increased DOPE was not only detected in the intestinal tract but also extended systemically and reflected in the central nervous system. Exogenous DOPE administration recapitulated the attenuation of experimental autoimmune encephalomyelitis pathogenesis by suppressing microglial activation. These findings highlight the therapeutic applicability of the microbiome and underscore its potential in human disease treatment.
PMID:
42448967
Bibliographic data and abstract were imported from PubMed on 15 Jul 2026.
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