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Zhou, Xiaohui

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Zhou

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Xiaohui

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Zhou, Xiaohui
Author's Publications: search.filters.isAuthorOfPublication.1aad5b23-497c-4301-81bb-238b5c3c088f

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    Comparative RNA-Seq based dissection of the regulatory networks and environmental stimuli underlying Vibrio parahaemolyticus gene expression during infection
    (Oxford University Press, 2014) Livny, Jonathan; Zhou, Xiaohui; Mandlik, Anjali; Hubbard, Troy P.; Davis, Brigid M.; Waldor, Matthew
    Vibrio parahaemolyticus is the leading worldwide cause of seafood-associated gastroenteritis, yet little is known regarding its intraintestinal gene expression or physiology. To date, in vivo analyses have focused on identification and characterization of virulence factors—e.g. a crucial Type III secretion system (T3SS2)—rather than genome-wide analyses of in vivo biology. Here, we used RNA-Seq to profile V. parahaemolyticus gene expression in infected infant rabbits, which mimic human infection. Comparative transcriptomic analysis of V. parahaemolyticus isolated from rabbit intestines and from several laboratory conditions enabled identification of mRNAs and sRNAs induced during infection and of regulatory factors that likely control them. More than 12% of annotated V. parahaemolyticus genes are differentially expressed in the intestine, including the genes of T3SS2, which are likely induced by bile-mediated activation of the transcription factor VtrB. Our analyses also suggest that V. parahaemolyticus has access to glucose or other preferred carbon sources in vivo, but that iron is inconsistently available. The V. parahaemolyticus transcriptional response to in vivo growth is far more widespread than and largely distinct from that of V. cholerae, likely due to the distinct ways in which these diarrheal pathogens interact with and modulate the environment in the small intestine.
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    Remodeling of the Intestinal Brush Border Underlies Adhesion and Virulence of an Enteric Pathogen
    (American Society of Microbiology, 2014) Zhou, Xiaohui; Massol, Ramiro H.; Nakamura, Fumihiko; Chen, Xiang; Gewurz, Benjamin E.; Davis, Brigid M.; Lencer, Wayne I.; Waldor, Matthew K.
    ABSTRACT Intestinal colonization by Vibrio parahaemolyticus—the most common cause of seafood-borne bacterial enteritis worldwide—induces extensive disruption of intestinal microvilli. In orogastrically infected infant rabbits, reorganization of the apical brush border membrane includes effacement of some microvilli and marked elongation of others. All diarrhea, inflammation, and intestinal pathology associated with V. parahaemolyticus infection are dependent upon one of its type 3 secretion systems (T3SS2); however, translocated effectors that directly mediate brush border restructuring and bacterial adhesion are not known. Here, we demonstrate that the effector VopV is essential for V. parahaemolyticus intestinal colonization and therefore its pathogenicity, that it induces effacement of brush border microvilli, and that this effacement is required for adhesion of V. parahaemolyticus to enterocytes. VopV contains multiple functionally independent and mechanistically distinct domains through which it disrupts microvilli. We show that interaction between VopV and filamin, as well as VopV’s previously noted interaction with actin, mediates enterocyte cytoskeletal reorganization. VopV’s multipronged approach to epithelial restructuring, coupled with its impact on colonization, suggests that remodeling of the epithelial brush border is a critical step in pathogenesis.
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    Inflammation and Disintegration of Intestinal Villi in an Experimental Model for \(Vibrio\) \(parahaemolyticus\)-Induced Diarrhea
    (Public Library of Science, 2012) Ritchie, Jennifer M.; Rui, Haopeng; Zhou, Xiaohui; Iida, Tetsuya; Kodoma, Toshio; Ito, Susuma; Davis, Brigid M.; Bronson, Roderick; Waldor, Matthew
    \(Vibrio\) \(parahaemolyticus\) is a leading cause of seafood-borne gastroenteritis in many parts of the world, but there is limited knowledge of the pathogenesis of \(V.\) \(parahaemolyticus\)-induced diarrhea. The absence of an oral infection-based small animal model to study \(V.\) \(parahaemolyticus\) intestinal colonization and disease has constrained analyses of the course of infection and the factors that mediate it. Here, we demonstrate that infant rabbits oro-gastrically inoculated with \(V.\) \(parahaemolyticus\) develop severe diarrhea and enteritis, the main clinical and pathologic manifestations of disease in infected individuals. The pathogen principally colonizes the distal small intestine, and this colonization is dependent upon type III secretion system 2. The distal small intestine is also the major site of \(V.\) \(parahaemolyticus\)-induced tissue damage, reduced epithelial barrier function, and inflammation, suggesting that disease in this region of the gastrointestinal tract accounts for most of the diarrhea that accompanies \(V.\) \(parahaemolyticus\) infection. Infection appears to proceed through a characteristic sequence of steps that includes remarkable elongation of microvilli and the formation of \(V.\) \(parahaemolyticus\)-filled cavities within the epithelial surface, and culminates in villus disruption. Both depletion of epithelial cell cytoplasm and epithelial cell extrusion contribute to formation of the cavities in the epithelial surface. \(V.\) \(parahaemolyticus\) also induces proliferation of epithelial cells and recruitment of inflammatory cells, both of which occur before wide-spread damage to the epithelium is evident. Collectively, our findings suggest that \(V.\) \(parahaemolyticus\) damages the host intestine and elicits disease via previously undescribed processes and mechanisms.