Electrogenic Ion Transport along the Human Duodenum in Childhood

One of the characteristic manifestations of Shiga-toxin-producing Escherichia coli (E. coli) infection in humans, including EHEC and Enteroaggregative E. coli O104:H4, is watery diarrhea. However, neither Shiga toxin nor numerous components of the type-3 secretion system have been found to independently elicit fluid secretion. We used the adult stem-cell-derived human colonoid monolayers (HCM) to test whether EHEC-secreted extracellular serine protease P (EspP), a member of the serine protease family broadly expressed by diarrheagenic E. coli can act as an enterotoxin. We applied the Ussing chamber/voltage clamp technique to determine whether EspP stimulates electrogenic ion transport indicated by a change in short-circuit current (Isc). EspP stimulates Isc in HCM. The EspP-stimulated Isc does not require protease activity, is not cystic fibrosis transmembrane conductance regulator (CFTR)-mediated, but is partially Ca2+-dependent. EspP neutralization with a specific antibody reduces its potency in stimulating Isc. Serine Protease A, secreted by Enteroaggregative E. coli, also stimulates Isc in HCM, but this current is CFTR-dependent. In conclusion, EspP stimulates colonic CFTR-independent active ion transport and may be involved in the pathophysiology of EHEC diarrhea. Serine protease toxins from E. coli pathogens appear to serve as enterotoxins, potentially significantly contributing to watery diarrhea.

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Evidence for an electrogenic ion transport pump in cells of higher plants

The Journal of Membrane Biology ◽

10.1007/bf01868016 ◽

1970 ◽

Vol 3 (1) ◽

pp. 210-222 ◽

Cited By ~ 70

Author(s):

N. Higinbotham ◽

J. S. Graves ◽

R. F. Davis

Keyword(s):

Ion Transport ◽

Higher Plants ◽

Electrogenic Ion Transport ◽

In Cells

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Cholinergic Modulation of Electrogenic Ion Transport in Different Regions of the Rat Small Intestine

Journal of Pharmacy and Pharmacology ◽

10.1111/j.2042-7158.1997.tb06094.x ◽

1997 ◽

Vol 49 (7) ◽

pp. 691-697 ◽

Cited By ~ 15

Author(s):

S. A. PRZYBORSKI ◽

R. J. LEVIN

Keyword(s):

Small Intestine ◽

Ion Transport ◽

Rat Small Intestine ◽

Cholinergic Modulation ◽

Electrogenic Ion Transport

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A PANI supported lipid bilayer that contains NhaA transporter proteins provides a basis for a biomimetic biocapacitor

Chemical Communications ◽

10.1039/c9cc05569j ◽

2019 ◽

Vol 55 (87) ◽

pp. 13152-13155

Author(s):

Awatef Ben Tahar ◽

Abdelkader Zebda ◽

Jean-Pierre Alcaraz ◽

Landry Gayet ◽

Abderrahim Boualam ◽

...

Keyword(s):

Ion Transport ◽

Lipid Bilayer ◽

High Speed ◽

Membrane System ◽

Transport Proteins ◽

Biological Engineering ◽

Supported Lipid Bilayer ◽

Transporter Proteins ◽

Electrogenic Ion Transport ◽

Biomimetic Membrane

This biomimetic membrane system of Na+/H+ transport proteins in a lipid bilayer supported by polyanaline has controllable electrogenic ion transport to function as a high-speed rechargeable biocapacitor for use in bioinspired biological engineering.

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Alterations to enteric neural signaling underlie secretory abnormalities of the ileum in experimental colitis in the guinea pig

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.90472.2008 ◽

2009 ◽

Vol 296 (4) ◽

pp. G717-G726 ◽

Cited By ~ 17

Author(s):

Ian M. Hons ◽

Joshua E. Burda ◽

John R. Grider ◽

Gary M. Mawe ◽

Keith A. Sharkey

Keyword(s):

Synaptic Transmission ◽

Ion Transport ◽

Action Potentials ◽

Experimental Colitis ◽

Trinitrobenzene Sulfonic Acid ◽

Contributing Factors ◽

Ileal Mucosa ◽

Ussing Chambers ◽

Electrogenic Ion Transport ◽

Secretomotor Neurons

Inflammatory bowel diseases (IBD) can involve widespread gastrointestinal dysfunction, even in cases in which inflammation is localized to a single site. The underlying pathophysiology of dysfunction in noninflamed regions is unclear. We examined whether colitis is associated with altered electrogenic ion transport in the ileal mucosa and/or changes in the properties of ileal submucosal neurons. Colitis was induced by administration of trinitrobenzene sulfonic acid (TNBS), and the uninflamed ileum from animals was examined 3, 7, and 28 days later. Electrogenic ion transport was assessed in Ussing chambers. Intracellular microelectrode recordings were used to examine the neurophysiology of the submucosal plexus of the ileum in animals with colitis. Noncholinergic secretion was reduced by 33% in the ileum from animals 7 days after the induction of colitis. The epithelial response to vasoactive intestinal peptide (VIP) was unaltered in animals with colitis, but the response to carbachol was enhanced. Slow excitatory synaptic transmission was dramatically reduced in VIP-expressing, noncholinergic secretomotor neurons. This change was detected as early as 3 days following TNBS treatment. No changes to fast synaptic transmission or the number of VIP neurons were observed. In addition, cholinergic secretomotor neurons fired more action potentials during a given stimulus, and intrinsic primary afferent neurons had broader action potentials in animals with colitis. These findings implicate changes to enteric neural circuits as contributing factors in inflammation-induced secretory dysfunction at sites proximal to a localized inflammatory insult.

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