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Epsilon toxin–producing Clostridium perfringens colonize the multiple sclerosis gut microbiome overcoming CNS immune privilege
Yinghua Ma, … , Christopher E. Mason, Timothy Vartanian
Yinghua Ma, … , Christopher E. Mason, Timothy Vartanian
Published February 28, 2023
Citation Information: J Clin Invest. 2023;133(9):e163239. https://doi.org/10.1172/JCI163239.
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Research Article Autoimmunity Microbiology

Epsilon toxin–producing Clostridium perfringens colonize the multiple sclerosis gut microbiome overcoming CNS immune privilege

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Abstract

Multiple sclerosis (MS) is a complex disease of the CNS thought to require an environmental trigger. Gut dysbiosis is common in MS, but specific causative species are unknown. To address this knowledge gap, we used sensitive and quantitative PCR detection to show that people with MS were more likely to harbor and show a greater abundance of epsilon toxin–producing (ETX-producing) strains of C. perfringens within their gut microbiomes compared with individuals who are healthy controls (HCs). Isolates derived from patients with MS produced functional ETX and had a genetic architecture typical of highly conjugative plasmids. In the active immunization model of experimental autoimmune encephalomyelitis (EAE), where pertussis toxin (PTX) is used to overcome CNS immune privilege, ETX can substitute for PTX. In contrast to PTX-induced EAE, where inflammatory demyelination is largely restricted to the spinal cord, ETX-induced EAE caused demyelination in the corpus callosum, thalamus, cerebellum, brainstem, and spinal cord, more akin to the neuroanatomical lesion distribution seen in MS. CNS endothelial cell transcriptional profiles revealed ETX-induced genes that are known to play a role in overcoming CNS immune privilege. Together, these findings suggest that ETX-producing C. perfringens strains are biologically plausible pathogens in MS that trigger inflammatory demyelination in the context of circulating myelin autoreactive lymphocytes.

Authors

Yinghua Ma, David Sannino, Jennifer R. Linden, Sylvia Haigh, Baohua Zhao, John B. Grigg, Paul Zumbo, Friederike Dündar, Daniel Butler, Caterina P. Profaci, Kiel Telesford, Paige N. Winokur, Kareem R. Rumah, Susan A. Gauthier, Vincent A. Fischetti, Bruce A. McClane, Francisco A. Uzal, Lily Zexter, Michael Mazzucco, Richard Rudick, David Danko, Evan Balmuth, Nancy Nealon, Jai Perumal, Ulrike Kaunzner, Ilana L. Brito, Zhengming Chen, Jenny Z. Xiang, Doron Betel, Richard Daneman, Gregory F. Sonnenberg, Christopher E. Mason, Timothy Vartanian

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Figure 7

ETX-EAE mice show increased CD68+ microglia in the cerebellum of ETX-EAE mice compared with PTX-EAE mice, despite similar activation in the spinal cord and a comparable profile of transcription factor NFκB p65 in both models.

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ETX-EAE mice show increased CD68+ microglia in the cerebellum of ETX-EAE...
(A) Representative sections from mice sacrificed at day 30 after immunization with CFA/MOG35-55 and followed by either ETX (ETX-EAE) or PTX (PTX-EAE) injections were immunostained with anti-CD68 antibody or anti-phospho-NFκB p65 (Ser 276). A rectangle-framed region in each condition in A is shown at a higher magnification beneath the corresponding section. SC, spinal cord; Ceb, cerebellum. Note that adjacent sections in each group were used for staining against CD68 and phospho-NFκB p65. Scale bars: 500 μm (bottom, spinal cord); 50 μm (top, spinal cord); 1 mm (bottom, cerebellum); 20 μm (top, cerebellum). (B–E) Statistical analysis of staining intensity for CD68 (A and B) and phosphor-NFκB p65 (pNFκB; D and E) in the spinal cord (B and D) and cerebellum (C and E), respectively. Data represent median range; Kruscal-Wallis test (nonparametric). NS, not significant. n = 4 and 8 mice for controls (Control: PBS > PTX; ETX: PBS > ETX-Hi) and EAE groups (PTX-EAE: MOG > PTX; ETX-EAE: MOG > ETX-Hi), respectively.

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ISSN: 0021-9738 (print), 1558-8238 (online)

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