Alimentary tractUltrastructural changes in the upper small intestinal mucosa in patients with cholera☆
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Cited by (63)
A dysbiotic gut microbiome suppresses antibody mediated-protection against Vibrio cholerae
2021, iScienceCitation Excerpt :Unlike other enteric pathogens such as Shigella and Salmonella, which cause clinically apparent inflammation and disease after penetrating cells or the intestinal epithelium, V. cholerae is thought to cause a non-inflammatory, noninvasive infection. However, cholera is associated with inflammatory changes such as widening of intracellular spaces, apical junction abnormalities as well as an infiltration of neutrophils, mast cells, and macrophages into the affected area (Mathan et al., 1995; Pulimood et al., 2008). Although innate immune cells such as neutrophils were shown to be essential for containment of V. cholerae, protection is mainly derived from adaptive immunity (Queen and Satchell, 2012).
Cholera immunity and development and use of oral cholera vaccines for disease control
2019, Mucosal Vaccines: Innovation for Preventing Infectious DiseasesInfections of the Gastrointestinal Tract
2018, Diagnostic Pathology of Infectious DiseaseVibrio cholerae OmpU induces IL-8 expression in human intestinal epithelial cells
2018, Molecular ImmunologyCitation Excerpt :Although intensive studies have been conducted on V. cholerae, less is known about the molecular mechanisms of V. cholerae-induced inflammatory responses because cholera has long been considered as a non-inflammatory disease (Farthing, 1997). However, recent works showed proinflammatory responses including infiltration of polymorphonuclear leukocytes, upregulation of lactoferrin, tumor necrosis factor-α, serum interleukin (IL)-6, and macrophage inhibitory protein-2 during natural cholera infection and in a pulmonary infection animal model (Fullner et al., 2002; Mathan et al., 1995; Qadri et al., 2004). Of these inflammatory mediators, Sarkar et al. reported increased expression of IL-8 upon V. cholerae infection in epithelial cells (Sarkar and Chaudhuri, 2004).
Cholera toxin disrupts barrier function by inhibiting exocyst-mediated trafficking of host proteins to intestinal cell junctions
2013, Cell Host and MicrobeCitation Excerpt :Cumulatively, these findings implicate Rab11-dependent endocytic recycling in maintaining normal intestinal barrier function and indicate that boosting this process offers protection against CT-dependent effects of V.c. infection. In the current study, we find that CtxA causes emaciation, disorganized junctions, and barrier disruption when expressed in the Drosophila midgut and contributes to lethality during infection of flies with V.c. Similarly, CT treatment produced apical gaps between epithelial cells in murine ileal loops, and histochemical staining and ultrastructural examination of CT-intoxicated human CACO-2 cells and Drosophila intestinal epithelial cells reveal parallel pathologies consisting of intercellular lacunae and convoluted borders between cells virtually identical to those observed in duodenal biopsies from human cholera patients (Mathan et al., 1995). Also, increased epithelial dye permeability has been reported in rats, mice, and rabbits following CT exposure (Magnusson et al., 1985; Ohishi and Odagiri, 1984; Triadafilopoulos et al., 1989), and serum albumin was found in the lumen of CT-treated rabbit ileal loops and in the stool of some cholera patients (De and Chatterje, 1953), which we too observed in CT-treated murine ileal loops.
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Supported by the Indian Council of Medical Research, the Wellcome Trust London, England, and the Rockefeller Foundation, New York, New York.