Ion transport in the experimental short bowel syndrome of the rat

Schulzke, Jörg–Dieter; Fromm, Michael; Bentzel, Carl J.; Zeitz, Martin; Menge, H.; Riecken, Ernst–Otto

doi:10.1016/0016-5085(92)90096-h

Cited by 69 publications

(33 citation statements)

References 29 publications

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“…Short-circuit current (I SC ) and transepithelial resistance (R t ) were determined by a computerized automatic clamp device (Fiebig Hard-and Software, Berlin, Germany). Mucosal-to-serosal (ms) mannitol flux studies were performed with [ 3 H]mannitol as described previously (39). Ion transport was determined by measurements of unidirectional (i.e., ms and serosal-to-mucosal [ms and sm, respectively]) 22 Na and 36 Cl fluxes (DuPont, Bad Homburg, Germany).…”

Section: Methodsmentioning

confidence: 99%

Aeromonas hydrophila Beta-Hemolysin Induces Active Chloride Secretion in Colon Epithelial Cells (HT-29/B6)

Epple¹,

Mankertz²,

Ignatius

et al. 2004

Infect Immun

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The diarrheal mechanisms in Aeromonas enteritis are not completely understood. In this study we investigated the effect of aeromonads and of their secretory products on ion secretion and barrier function of monolayers of human intestinal cells (HT-29/B6). Ion secretion was determined as a short-circuit current (I SC ) of HT-29/B6 monolayers mounted in Ussing-type chambers. Transepithelial resistance (R t ) served as a measure of permeability. A diarrheal strain of Aeromonas hydrophila (strain Sb) added to the mucosal side of HT-29/B6 monolayers induced a significant I SC (39 ؎ 3 A/cm 2 ) and decreased the R t to ϳ10% of the initial value. A qualitatively identical response was obtained with sterile supernatant of strain Sb, and Aeromonas supernatant also induced a significant I SC in totally stripped human colon. Tracer flux and ion replacement studies revealed the I SC to be mainly accounted for by electrogenic Cl ؊ secretion. Supernatant applied serosally completely abolished basal I SC . The supernatant-induced I SC was inhibited by the protein kinase C inhibitor chelerythrine, whereas a protein kinase A inhibitor (H8) and a Ca 2؉ chelator (BAPTA-AM) had no effect. Physicochemical properties indicated that the supernatant's active compound was an aerolysin-related Aeromonas betahemolysin. Accordingly, identical I SC and R t responses were obtained with Escherichia coli lysates harboring the cloned beta-hemolysin gene from strain SB or the aerA gene encoding for aerolysin. Sequence comparison revealed a 64% homology between aerolysin and the beta-hemolysin cloned from Aeromonas sp. strain Sb. In conclusion, beta-hemolysin secreted by pathogenic aeromonads induces active Cl ؊ secretion in the intestinal epithelium, possibly by channel insertion into the apical membrane and by activation of protein kinase C.Numerous reports have implicated Aeromonas species as a cause of human enteric disease in children as well as in adults (for reviews, see references 3, 22, 23, 28, and 36). However, although a large body of literature on Aeromonas virulence factors has been accumulated (for a review, see references 9 and 22), the mechanisms of the diarrheic action of Aeromonas are not completely understood. As for other pathogens, Aeromonas virulence factors can be divided into cellular properties such as adherence, invasiveness, motility, and extracellular factors secreted by pathogenic aeromonads (22). Evidence for the enteropathogenic potential of these virulence factors was obtained from their epidemiological association with diarrheal disease (3,10,24), from their ability to induce enteral fluid secretion in animal models, and from the observation of effects linked to enteral fluid secretion elicited in various animal and cell culture systems (see, for example, references 4, 7, 29, and 33). Surprisingly, then, the precise mechanism for how Aeromonas infection causes intestinal fluid secretion has not yet been elucidated.From a general pathophysiological point of view, intestinal pathogens can induce diarrhea by induction...

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Section: Methodsmentioning

confidence: 99%

Aeromonas hydrophila Beta-Hemolysin Induces Active Chloride Secretion in Colon Epithelial Cells (HT-29/B6)

Epple¹,

Mankertz²,

Ignatius

et al. 2004

Infect Immun

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“…To determine transcellular electroneutral NaCl transport and paracellular solute transport in the proximal colon, measurements of unidirectional fluxes with 22 Na ϩ , 36 Cl Ϫ , and [ 3 H]mannitol were performed. All experiments were performed under short-circuit conditions as described previously (47). Voltage, short-circuit current (Isc), and electrical resistance were measured by using a computercontrolled voltage clamp device (CVC 6; Fiebig, Berlin, Germany).…”

Section: Animals and Tissue Preparation Il-2mentioning

confidence: 99%

“…This correction, applied to bath resistance, is well accepted, but it is also necessary to correct I sc and net fluxes for the R sub of intestinal preparations. The implications of this correction have previously been provided (15,22,47,48,51). Generally, after correction for the bathing solution, the true active transport rate becomes underestimated by a factor that is given by the ratio of R t and R e .…”

Section: G247mentioning

confidence: 99%

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Mechanisms of diarrhea in the interleukin-2-deficient mouse model of colonic inflammation

Barmeyer¹,

Harren²,

Schmitz³

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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Colitis in interleukin-2-deficient (IL-2-/-) mice resembles ulcerative colitis in humans. We studied epithelial transport and barrier function in IL-2-/- mice and used this model to characterize mechanisms of diarrhea during intestinal inflammation. 22Na+ and 36Cl- fluxes were measured in proximal colon. Net Na+ flux was reduced from 4.0 ± 0.5 to 0.8 ± 0.5 μmol·h-1·cm-2, which was paralleled by diminished mRNA and protein expression of the Na+/H+ exchanger NHE3. Net Cl- flux was also decreased from 2.2 ± 1.6 to -2.7 ± 0.6 μmol·h-1·cm-2, indicating impaired Na+-Cl- absorption. In distal colon, aldosterone-induced electrogenic Na+ absorption was 6.1 ± 0.9 μmol·h-1·cm-2 in controls and was abolished in IL-2-/- mice. Concomitantly, mRNA expression of β- and γ-subunits of the epithelial sodium channel (ENaC) was reduced. Epithelial barrier was studied in proximal colon by impedance technique and mannitol fluxes. In contrast to ulcerative colitis, epithelial resistance was increased and mannitol fluxes were decreased in IL-2-/- mice. This was in accord with the findings of reduced ion transport as well as increased expression of tight junction proteins occludin and claudin-1, -2, -3, and -5. In conclusion, the IL-2-/- mucosa exhibits impaired electroneutral Na+-Cl- absorption and electrogenic Na+ transport due to reduced mRNA and protein expression of NHE3 and ENaC β- and γ-subunit mRNA. This represents a model of early intestinal inflammation with absorptive dysfunction due to impaired transport protein expression/function while epithelial barrier is still intact. Therefore, this model is ideal to study regulation of transporter expression independent of barrier defects.

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“…After massive small bowel resection, the residual intestine has the compensatory ability to adapt by cellular hyperplasia and increased absorptive function [1,2]. Many factors including luminal nutrients and hormones modulate the adaptive response [3,4].…”

mentioning

confidence: 99%

Altered small intestinal absorptive enzyme activities in leptin-deficient obese mice: influence of bowel resection

Kiely

Noh

Svatek

et al. 2006

Journal of Pediatric Surgery

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Ion transport in the experimental short bowel syndrome of the rat

Cited by 69 publications

References 29 publications

Aeromonas hydrophila Beta-Hemolysin Induces Active Chloride Secretion in Colon Epithelial Cells (HT-29/B6)

Aeromonas hydrophila Beta-Hemolysin Induces Active Chloride Secretion in Colon Epithelial Cells (HT-29/B6)

Mechanisms of diarrhea in the interleukin-2-deficient mouse model of colonic inflammation

Altered small intestinal absorptive enzyme activities in leptin-deficient obese mice: influence of bowel resection

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