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Isolation of Clostridium perfringens type B in an individual at first clinical presentation of multiple sclerosis provides clues for environmental triggers of the disease.

TitleIsolation of Clostridium perfringens type B in an individual at first clinical presentation of multiple sclerosis provides clues for environmental triggers of the disease.
Publication TypeJournal Article
Year of Publication2013
AuthorsRumah KRashid, Linden J, Fischetti VA, Vartanian T
JournalPLoS One
Volume8
Issue10
Paginatione76359
Date Published2013
ISSN1932-6203
KeywordsAdult, Bacterial Toxins, Brain, Case-Control Studies, Clostridium perfringens, Endothelial Cells, Environment, Female, Humans, Lupus Erythematosus, Systemic, Magnetic Resonance Imaging, Male, Middle Aged, Multiple Sclerosis, Myelin Sheath, Prevalence, Protein Binding, Retinal Vessels, Young Adult
Abstract

We have isolated Clostridium perfringens type B, an epsilon toxin-secreting bacillus, from a young woman at clinical presentation of Multiple Sclerosis (MS) with actively enhancing lesions on brain MRI. This finding represents the first time that C. perfringens type B has been detected in a human. Epsilon toxin's tropism for the blood-brain barrier (BBB) and binding to oligodendrocytes/myelin makes it a provocative candidate for nascent lesion formation in MS. We examined a well-characterized population of MS patients and healthy controls for carriage of C. perfringens toxinotypes in the gastrointestinal tract. The human commensal Clostridium perfringens type A was present in approximately 50% of healthy human controls compared to only 23% in MS patients. We examined sera and CSF obtained from two tissue banks and found that immunoreactivity to ETX is 10 times more prevalent in people with MS than in healthy controls, indicating prior exposure to ETX in the MS population. C. perfringens epsilon toxin fits mechanistically with nascent MS lesion formation since these lesions are characterized by BBB permeability and oligodendrocyte cell death in the absence of an adaptive immune infiltrate.

DOI10.1371/journal.pone.0076359
Alternate JournalPLoS ONE
PubMed ID24146858
PubMed Central IDPMC3797790
Grant ListT32 GM007739 / GM / NIGMS NIH HHS / United States

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