In vivo study reveals Citrobacter rodentium alters host cholesterol transport and depletes commensal bacteria, suggesting pathogen-driven metabolic remodeling.
and a reduction in colon-associated anaerobic commensals. In addition, IECs responded to infection by activating Srebp2 and the cholesterol biosynthetic pathway. Unexpectedly, infected IECs also upregulated the cholesterol efflux proteins AbcA1, AbcG8, and ApoA1, resulting in higher levels of fecal cholesterol and a bloom of Proteobacteria. These results suggest that C. rodentium manipulates host metabolism to evade innate immune responses and establish a favorable gut ecosystem.
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Berger et al. (2017) studied this question.
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