Вторичный метаболит Лимосилактобыциллусретери R2lc движет специфической патологией штамма в спонтанной модели мыши множественного склероза.
Обработка статьи · этапы, ошибки и управление
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Archer Dale, Pérez-Muñoz María Elisa, Tollenaar Stephanie, Veniamin Simona, Hotte Naomi, Cheng Christopher C, Nieves Kristoff, Oh Jee-Hwan, Morceli Lilian, Muncner Susan, Barreda Daniel R, Krishnamoorthy Gurumoorthy, Power Christopher, van Pijkeren Jan-Peter, Walter Jens
Аннотация
Оригинал публикации
A secondary metabolite of Limosilactobacillusreuteri R2lc drives strain-specific pathology in a spontaneous mouse model of multiple sclerosis.
Limosilactobacillus reuteri is an immunomodulatory bacterium enriched in non-industrialized microbiomes, making it a therapeutic candidate for chronic diseases. However, effects of L. reuteri strains in mouse models of multiple sclerosis have been contradictory. Here, we show that treatment of spontaneous relapsing-remitting experimental autoimmune encephalomyelitis (EAE) mice with L. reuteri R2lc, a strain that activates the aryl hydrocarbon receptor (AhR) through the pks gene cluster, resulted in severe pathology. In contrast, a pks mutant and a pks-negative strain (PB-W1) failed to exacerbate EAE and exhibited reduced pathology compared to R2lc despite earlier disease onset in PB-W1 mice. Differences in pathology occurred in parallel with a pks-dependent downregulation of AhR-related genes, reduced occludin expression in the forebrain, and altered concentrations of immune cells. This work establishes a molecular foundation for strain-specific effects on autoimmunity, which has implications for our understanding of how microbes contribute to chronic conditions and the selection of microbial therapeutics.