Publications by authors named "G I Sandle"

Mesenteric ischemia increases gut permeability and bacterial translocation. In human colon, chemical hypoxia induced by 2,4-dinitrophenol (DNP) activates basolateral intermediate conductance K (IK) channels (designated KCa3.1 or KCNN4) and increases paracellular shunt conductance/permeability (), but whether this leads to increased macromolecule permeability is unclear.

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Diarrhea, often severe, is a recognized and frequently early symptom during acute COVID-19 infection and may persist or develop for the first time in patients with long-COVID, with socioeconomic consequences. Diarrheal mechanisms in these cases are poorly understood. There is evidence for disruption of intestinal epithelial barrier function and also for changes in the gut microbiome, which is critical for gut immunity and metabolism.

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Infections by the zoonotic foodborne bacterium () are among the most frequent causes of bacterial gastroenteritis worldwide. The aim was to evaluate the relationship between epithelial barrier disruption, mucosal immune activation, and vitamin D (VD) treatment during infection, using intestinal epithelial cells and mouse models focused on the interaction of with the VD signaling pathway and VD treatment to improve -induced barrier dysfunction. Our RNA-Seq data from campylobacteriosis patients demonstrate inhibition of VD receptor (VDR) downstream targets, consistent with suppression of immune function.

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Intermediate conductance potassium (IK) channels are exquisitively Ca sensitive, intracellular Ca regulating channel activity by complexing with calmodulin (CaM), which is bound to the cytosolic carboxyl tail. Although CaM antagonists might be expected to decrease IK channel activity, the effect of W-7 in human T lymphocytes are conflicting. We therefore evaluated the effect of W-7 on basolateral IK channels in human colonic crypt cells.

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Transepithelial K absorption requires apical K uptake and basolateral K exit. In the colon, apical H-K-ATPase mediates cellular K uptake, and it has been suggested that electroneutral basolateral K exit reflects K-Cl cotransporter-1 (KCC1) operating in parallel with K and Cl channels. The present study was designed to identify basolateral transporter(s) responsible for K exit in rat distal colon.

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