Characterising barrier function among regions of the gastrointestinal tract in Holstein steers

2014 ◽  
Vol 54 (9) ◽  
pp. 1282 ◽  
Author(s):  
G. B. Penner ◽  
J. R. Aschenbach ◽  
K. Wood ◽  
M. E. Walpole ◽  
R. Kanafany-Guzman ◽  
...  
Keyword(s):  
Gastrointestinal Tract ◽  
Barrier Function ◽  
Short Circuit ◽  
Ussing Chamber ◽  
Distal Colon ◽  
Proximal Colon ◽  
Flux Rate ◽  
Buffer Solution ◽  
Solution Ph ◽  
Mannitol Flux

The objective of this study was to characterise the regional variation in the barrier function of the gastrointestinal tract in Holstein calves using the flux rates of mannitol and inulin as permeability markers and tissue conductance (Gt) as an electrophysiological indicator of barrier function. Six Holstein steer calves (6 months of age) fed a common diet were used. Calves were killed by captive bolt stunning and pithing, and tissues were collected from the rumen, omasum, duodenum, jejunum, ileum, caecum, proximal colon, and distal colon. Tissues were carefully washed using a pre-heated (38.5°C) buffer solution (pH 7.4) saturated with oxygen and then transported to the laboratory. The mucosa was prepared by hand stripping and mounted between two halves of an Ussing chamber (n = 3/region with an exposed surface area of 3.14 cm2 for rumen and omasum and 1 cm2 for all other tissues). All tissues were incubated under short-circuit conditions and exposed to a similar buffer solution except for the energy source; rumen, omasum, caecum, and colon tissues were incubated with buffer containing short-chain fatty acids while tissues from the small intestine were bathed in buffer containing glucose. The Gt and the serosal-to-mucosal flux rates of 14C-inulin and 3H-mannitol were measured as indicators of barrier function. The serosal-to-mucosal flux rate of mannitol was greatest (P < 0.001) in the jejunum [104.8 nmol/(cm2 × h)] and least in the rumen and omasum [20.3 and 18.6 nmol/(cm2 × h), respectively]. In contrast, the serosal-to-mucosal flux rate of inulin was greatest (P < 0.001) in the omasum [158.6 nmol/(cm2 × h)] followed by the rumen [87.3 nmol/(cm2 × h)] with no differences among the other regions [18.7 – 62.0 nmol/(cm2 × h)]. The Gt was greatest (P < 0.001) in the jejunum (34.6 mS/cm2) and least for the rumen (3.67 mS/cm2) and omasum (3.23 mS/cm2). The Gt was correlated with both inulin and mannitol flux rates in duodenum, caecum and proximal colon (P < 0.05); whereas, no such correlations existed in jejunum, ileum and distal colon. The Gt was correlated with the mannitol flux rate but not the inulin flux rate in rumen and omasum. For all regions but the rumen and omasum there was a positive correlation between mannitol and inulin flux rates. These data indicate that the translocation of a large molecule (inulin) across the omasum and rumen is greatest despite having an apparently tight epithelium based on Gt and mannitol flux rate, while the jejunum appears to have greatest potential for paracellular permeability.

scholarly journals Segment-specific effects of epinephrine on ion transport in the colon of the rat

1998 ◽  
Vol 275 (6) ◽  
pp. G1367-G1376 ◽  
Author(s):  
Silke Hörger ◽  
Gerhard Schultheiß ◽  
Martin Diener
Keyword(s):  
Ion Transport ◽  
Short Circuit ◽  
Ussing Chamber ◽  
Short Circuit Current ◽  
Distal Colon ◽  
Proximal Colon ◽  
Rat Colon ◽  
Second Phase ◽  
Stimulatory Action ◽  
Β Receptor

The effect of epinephrine on transport of K+, Na+, Cl−, and[Formula: see text] across the rat colon was studied using the Ussing chamber technique. Epinephrine (5 × 10−6mol/l) induced a biphasic change in short-circuit current ( Isc) in distal and proximal colon: a transient increase followed by a long-lasting decay. The first phase of the Iscresponse was abolished in Cl−-poor solution or after bumetanide administration, indicating a transient induction of Cl−secretion. The second phase of the response to epinephrine was suppressed by apical administration of the K+channel blocker, quinine, and was concomitant with an increase in serosal-to-mucosal Rb+flux, indicating that epinephrine induced K+secretion, although this response was much smaller than the change in Isc. In addition, the distal colon displayed a decrease in mucosal-to-serosal and serosal-to-mucosal Cl−fluxes when treated with epinephrine. In the distal colon, indomethacin abolished the first phase of the epinephrine effect, whereas the second phase was suppressed by TTX. In the proximal colon, indomethacin and TTX were ineffective. The neuronally mediated response to epinephrine in the distal colon was suppressed by the nonselective β-receptor blocker, propranolol, and by the β2-selective blocker, ICI-118551, whereas the epithelial response in the proximal colon was suppressed by the nonselective α-blocker, phentolamine, and by the selective α2-blocker, yohimbine. These results indicate a segment-specific action of epinephrine on ion transport: a direct stimulatory action on epithelial α2-receptors in the proximal colon and an indirect action on secretomotoneurons via β2-receptors in the distal colon.

Dietary flavonol quercetin induces chloride secretion in rat colon

1998 ◽  
Vol 275 (5) ◽  
pp. G1166-G1172 ◽  
Author(s):  
Rainer Cermak ◽  
Ursula Föllmer ◽  
Siegfried Wolffram
Keyword(s):  
Short Circuit ◽  
Ussing Chamber ◽  
Phosphodiesterase Inhibitor ◽  
Short Circuit Current ◽  
Distal Colon ◽  
Chloride Secretion ◽  
Proximal Colon ◽  
Rat Colon ◽  
Quercetin Glycoside

The aim of this study was to investigate the possible effects of the flavonol quercetin, the most abundant dietary flavonoid, on the intestinal mucosa. In vitro experiments were performed with various segments of the rat intestine, using the Ussing chamber technique. Quercetin increased the short-circuit current ( I sc) in the jejunum, ileum, and proximal and distal colon. Additional experiments were performed using preparations of the proximal colon. The maximum effective dose of quercetin was found to be ∼100 μM. The quercetin-induced increase in I sc was inhibited by the Cl− channel blocker 5-nitro-2-(3-phenylpropylamino)-benzoic acid. Adding blockers of the Na+-K+-2Cl−cotransporter to the serosal compartment diminished the increase of I sc due to quercetin. Ion substitution and flux measurements indicated that the effect of quercetin was due to electrogenic Cl− and[Formula: see text] secretion. In contrast to the aglycone, the quercetin glycoside rutin had no effect. The effect of quercetin on I scwas additive to the I sc increase induced by forskolin, but the flavonoid diminished the I sc evoked by carbachol. The phosphodiesterase inhibitor theophylline blocked the effect of quercetin. Genistein, a related isoflavone, did not alter the I sc evoked by quercetin. These findings demonstrate that the dietary flavonol quercetin induces Cl−secretion and most likely [Formula: see text]secretion in rat small and large intestine. The effects are restricted to the flavonol aglycone.

Control of electrogenic Na+ absorption in rat late distal colon by nanomolar aldosterone added in vitro

1993 ◽  
Vol 264 (1) ◽  
pp. E68-E73 ◽  
Author(s):  
M. Fromm ◽  
J. D. Schulzke ◽  
U. Hegel
Keyword(s):  
Short Circuit ◽  
Ussing Chamber ◽  
Short Circuit Current ◽  
Distal Colon ◽  
Proximal Colon ◽  
Hill Coefficient ◽  
Late Response ◽  
Maximal Velocity ◽  
Time Courses

It has been possible to obtain in a mammalian epithelium of dietetically and surgically untreated animals a dose response of in vitro-added aldosterone (Aldo, 10(-10) to 10(-5) M) on electrogenic Na+ absorption (JeNa). JeNa was measured in the Ussing chamber on stripped rat late distal colon 8 h after in vitro addition of Aldo. Submaximal effects were obtained at 3 nM Aldo; after a lag time of 2 h, short-circuit current (Isc) increased to a maximum of 234 +/- 15 microA/cm2 and dropped after 0.1 mM amiloride to -18 +/- 3 microA/cm2, resulting in JeNa of 9.4 +/- 0.6 mumol.h-1 x cm-1. Net Na+ tracer fluxes and Isc exhibited parallel time courses, so that electroneutral Na+ transport was not induced in late distal colon by acute Aldo. A plot of JeNa vs. Na conductance revealed an electromotive force (ENa) of 126 +/- 1 mV for all Aldo concentrations tested. Kinetic data were as follows: Michaelis constant 1.2 nM, maximal velocity (Vmax) 10.5 mumol.h-1 x cm-2, and Hill coefficient 2.1. In contrast to the large effect in late distal colon, 3 nM Aldo caused JeNa of < 1 mumol.h-1 x cm-2 in early distal colon, proximal colon, and cecum. Antimineralocorticoid sensitivity and ENa did not vary with Aldo concentration or time of the experiment, consistent with a unique mechanism during the early and late response up to 8 h, as well as at mineralocorticoid and glucocorticoid Aldo concentrations. Acute Aldo in a range of 0.1–10 nM fully controls JeNa between zero and Vmax in late distal colon.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Effect of ruminal acidosis and short-term low feed intake on indicators of gastrointestinal barrier function in Holstein steers

2018 ◽  
Vol 96 (1) ◽  
pp. 108-125 ◽  
Author(s):  
Rae-Leigh A Pederzolli ◽  
Andrew G Van Kessel ◽  
John Campbell ◽  
Steve Hendrick ◽  
Katie M Wood ◽  
...  
Keyword(s):  
Barrier Function ◽  
Distal Colon ◽  
Proximal Colon ◽  
Cell Junction ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Ruminal Acidosis ◽  
Junction Protein ◽  
Ad Libitum ◽  
Ad Libitum Intake

Abstract The objective of this study was to determine effect of ruminal acidosis (RA) and low feed intake [LFI] on the regional barrier function of the gastrointestinal tract. Twenty-one Holstein steers were fed for ad libitum intake for 5 d (control [CON]), fed at 25% of ad libitum intake for 5 d (LFI), or provided 2 d of ad libitum intake followed by 1-d of feed restriction (25% of ad libitum intake), 1 d where 30% of ad libitum dry matter intake (DMI) was provided as pelleted barley followed by the full allocation (RA) and fed for ad libitum intake the following day. Tissues and digesta from the rumen, omasum, duodenum, jejunum, ileum, cecum, proximal, and distal colon were collected. Permeability was assessed using the mucosal-to-serosal flux of inulin (JMS-inulin) and mannitol (JMS-mannitol). Digesta pH was 0.81, 0.63, and 0.42 pH units less for RA than CON in the rumen, cecum, and proximal colon; while, LFI had pH that was 0.47 and 0.36 pH units greater in the rumen and proximal colon compared to CON. Total ruminal short-chain fatty acid (SCFA) concentration were less for LFI (92 mM; P = 0.010) and RA (87 mM; P = 0.007) than CON (172 mM) steers. In the proximal colon, the proportion of butyrate (P = 0.025 and P = 0.022) and isobutyrate (P = 0.019 and P = 0.019) were greater, and acetate (P = 0.028 and P = 0.028) was less for LFI and RA, respectively, when compared to CON steers. Ruminal papillae length, width, perimeter, and surface area were 1.21 mm, 0.78 mm, 3.84 mm, and 11.15 mm2 less for LFI than CON; while, RA decreased papillae width by 0.52 mm relative to CON. The JMS-mannitol was less for LFI steers than CON in the proximal colon (P = 0.041) and in the distal colon (P = 0.015). Increased gene expression for claudin 1, occludin, tight-cell junction protein 1 and 2, and toll-like receptor 4 were detected for LFI relative to CON in the rumen, jejunum, and proximal colon. For RA steers, expression of toll-like receptor 4 in the rumen, and occludin and tight-cell junction protein 1 were greater in the jejunum than CON. An acute RA challenge decreased pH in the rumen and large intestine but did not increase tissue permeability due to increases in the expression of genes related to barrier function within 1 d of the challenge. Steers exposed to LFI for 5 d had reduced ruminal SCFA concentrations, smaller ruminal papillae dimensions, and increased tissue permeability in the proximal and distal colon despite increases for genes related to barrier function and immune function.

Ion transport by neonatal rabbit distal colon

1986 ◽  
Vol 250 (6) ◽  
pp. G754-G759 ◽  
Author(s):  
G. D. Potter ◽  
S. M. Burlingame
Keyword(s):  
Small Intestine ◽  
Short Circuit ◽  
Ussing Chamber ◽  
Electrical Conductance ◽  
Short Circuit Current ◽  
Distal Colon ◽  
Ion Fluxes ◽  
Adult Rabbit ◽  
Rabbit Colon ◽  
Edge Damage

The neonatal small intestine is characterized by electrical conductance and permeability to ions higher than in the corresponding adult intestine. To investigate whether this property of the neonate is limited to the small intestine, or extends to the colon, a modified Ussing chamber for determination of transmucosal potential difference (PD), short-circuit current (Isc), transepithelial conductance (Gt), and ion fluxes in the neonatal rabbit distal colon was constructed. After care to reduce edge damage, Gt for the neonatal colon was found to be 8.4 +/- 0.3 mS . cm2 and for adult colon in the same chamber, 7.4 +/- 0.5 (P greater than 0.05). Net Na and Cl fluxes under short-circuit conditions were similar to those obtained in adult colon. Unidirectional ion fluxes were also similar to those of the adult. Net Na flux (JNanet) was incompletely inhibited by 10(-4) M of amiloride. Response to replacement of Na, Cl, and HCO3-, respectively, in the bathing solutions was not different from that expected in adult rabbit colon. Thus differences between adult and neonatal rabbit colon were small, and the increased conductance and unidirectional ion fluxes characteristic of the neonatal small intestine were not evident in the neonatal rabbit distal colon.

Modulation of secretagogue-induced chloride secretion by intracellular bicarbonate

1994 ◽  
Vol 266 (5) ◽  
pp. G929-G934 ◽  
Author(s):  
P. C. Dagher ◽  
T. Z. Morton ◽  
C. S. Joo ◽  
A. Taglietta-Kohlbrecher ◽  
R. W. Egnor ◽  
...  
Keyword(s):  
Cell Line ◽  
Short Circuit ◽  
Ussing Chamber ◽  
Tumor Cell Line ◽  
Distal Colon ◽  
Rat Colon ◽  
Sprague Dawley ◽  
T84 Cells ◽  
Cl Secretion ◽  
Rat Distal Colon

We have previously demonstrated inhibition of basal Cl- secretion by intracellular bicarbonate concentration ([HCO3-]i) in rat distal colon. We now examined whether secretagogue-induced Cl- secretion is inhibited by [HCO3-]i as well. Stripped segments of distal colon from male Sprague-Dawley rats and the colon tumor cell line T84 were studied. Flux measurements were performed in the Ussing chamber under short-circuit conditions. [HCO3-]i was calculated from intracellular pH (pHi) values that were estimated with the pH-sensitive dye 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein. Dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP) and carbachol were used as secretagogues. In both distal colon and T84 cells, [HCO3-]i did not affect cAMP-induced Cl- secretion. However, carbachol-induced secretion was inhibited by [HCO3-]i; in rat colon, Cl- secretion decreased from 2.3 to 1.5 mueq.cm-2.h-1 when [HCO3-]i was increased from 15.0 to 28.4 mM (P < 0.05). In T84 cells, the change in short-circuit current decreased from 8.1 to 1.1 microA/cm2 over a range of [HCO3-]i from 0 to 15.6 mM (P < 0.001). We conclude that [HCO3-]i is an important modulator of carbachol-stimulated Cl- secretion in both rat distal colon and the T84 cell line. cAMP-mediated secretion is not affected by [HCO3-]i.

Acid-base effects on electrolyte transport in CA II-deficient mouse colon

2000 ◽  
Vol 278 (3) ◽  
pp. G409-G415 ◽  
Author(s):  
David S. Goldfarb ◽  
William S. Sly ◽  
Abdul Waheed ◽  
Alan N. Charney
Keyword(s):  
Short Circuit ◽  
Ussing Chamber ◽  
Distal Colon ◽  
Ringer Solution ◽  
Electrolyte Transport ◽  
Western Blots ◽  
Effects Of Ph ◽  
Membrane Bound ◽  
Ph Decrease

To determine the role of carbonic anhydrase (CA) in colonic electrolyte transport, we studied Car-2 0 mice, mutants deficient in cytosolic CA II. Ion fluxes were measured under short-circuit conditions in an Ussing chamber. CA was analyzed by assay and Western blots. In Car-2 0 mouse colonic mucosa, total CA activity was reduced 80% and cytosolic CA I and membrane-bound CA IV activities were not increased. Western blots confirmed the absence of CA II in Car-2 0 mice. Normal mouse distal colon exhibited net Na+ and Cl− absorption, a serosa-positive PD, and was specifically sensitive to pH. Decrease in pH stimulated active Na+ and Cl− absorption whether it was caused by increasing solution [Formula: see text], reducing [Formula: see text] concentration, or reducing pH in CO2/[Formula: see text]-free HEPES-Ringer solution. Membrane-permeant methazolamide, but not impermeant benzolamide, at 0.1 mM prevented the effects of pH. Car-2 0 mice exhibited similar basal transport rates and responses to pH and CA inhibitors. We conclude that basal and pH-stimulated colonic electrolyte absorption in mice requires CA I. CA II and IV may have accessory roles.

Cyclic nucleotide-gated cation channels mediate sodium and calcium influx in rat colon

2000 ◽  
Vol 278 (2) ◽  
pp. C336-C343 ◽  
Author(s):  
W. Qiu ◽  
B. Lee ◽  
M. Lancaster ◽  
W. Xu ◽  
S. Leung ◽  
...  
Keyword(s):  
Cyclic Nucleotide ◽  
Calcium Absorption ◽  
Calcium Influx ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Distal Colon ◽  
Proximal Colon ◽  
Cation Channels ◽  
Rat Colon ◽  
Sodium Absorption

We found mRNA for the three isoforms of the cyclic nucleotide-gated nonselective cation channel expressed in the mucosal layer of the rat intestine from the duodenum to the colon and in intestinal epithelial cell lines in culture. Because these channels are permeable to sodium and calcium and are stimulated by cGMP or cAMP, we measured 8-bromo-cGMP-stimulated sodium-mediated short-circuit current ( I sc) in proximal and distal colon and unidirectional45Ca2+fluxes in proximal colon to determine whether these channels could mediate transepithelial sodium and calcium absorption across the colon. Sodium-mediated I sc, stimulated by 8-bromo-cGMP, were inhibited by dichlorobenzamil and l-cis-diltiazem, blockers of cyclic nucleotide-gated cation channels, suggesting that these ion channels can mediate transepithelial sodium absorption. Sodium-mediated I sc and net transepithelial45Ca2+absorption were stimulated by heat-stable toxin from Escherichia coli that increases cGMP. Addition of l-cis-diltiazem inhibited the enhanced transepithelial absorption of both ions. These results suggest that cyclic nucleotide-gated cation channels simultaneously increase net sodium and calcium absorption in the colon of the rat.

Effects of carbon monoxide on ion transport across rat distal colon

2011 ◽  
Vol 300 (2) ◽  
pp. G207-G216 ◽  
Author(s):  
Julia Steidle ◽  
Martin Diener
Keyword(s):  
Carbon Monoxide ◽  
Ion Transport ◽  
Short Circuit ◽  
Ussing Chamber ◽  
Short Circuit Current ◽  
Distal Colon ◽  
Disulfonic Acid ◽  
Maximal Response ◽  
Colonic Crypts ◽  
Acid Sodium Salt

The aim of the present study was to investigate whether carbon monoxide (CO) induces changes in ion transport across the distal colon of rats and to study the mechanisms involved. In Ussing chamber experiments, tricarbonyldichlororuthenium(II) dimer (CORM-2), a CO donor, evoked a concentration-dependent increase in short-circuit current ( Isc). A maximal response was achieved at a concentration of 2.5·10−4 mol/l. Repeated application of CORM-2 resulted in a pronounced desensitization of the tissue. Anion substitution experiments suggest that a secretion of Cl− and HCO3− underlie the CORM-2-induced current. Glibenclamide, a blocker of the apical cystic fibrosis transmembrane regulator channel, inhibited the Isc induced by the CO donor. Similarly, bumetanide, a blocker of the basolateral Na+-K+-2Cl− cotransporter, combined with 4-acetamido-4′-isothiocyanato-stilbene-2,2′-disulfonic acid sodium salt, an inhibitor of the basolateral Cl−/HCO3− exchanger, inhibited the CORM-2-induced Isc. Membrane permeabilization experiments indicated an activation of basolateral K+ and apical Cl− channels by CORM-2. A partial inhibition by the neurotoxin, tetrodotoxin, suggests the involvement of secretomotor neurons in this response. In imaging experiments at fura-2-loaded colonic crypts, CORM-2 induced an increase of the cytosolic Ca2+ concentration. This increase depended on the influx of extracellular Ca2+, but not on the release of Ca2+ from intracellular stores. Both enzymes for CO production, heme oxygenase I and II, are expressed in the colon as observed immunohistochemically and by RT-PCR. Consequently, endogenous CO might be a physiological modulator of colonic ion transport.

scholarly journals SARS-COV-2 induced Diarrhea is inflammatory, Ca2+ Dependent and involves activation of calcium activated Cl channels

2021 ◽  
Author(s):  
Mark Donowitz ◽  
Chung-Ming Tse ◽  
Karol Dokladny ◽  
Manmeet Rawat ◽  
Ivy Horwitz ◽  
...  
Keyword(s):  
Short Circuit ◽  
Ussing Chamber ◽  
Short Circuit Current ◽  
Proximal Colon ◽  
K Channel ◽  
Mrna Levels ◽  
Apical Surface ◽  
Live Virus ◽  
Anion Secretion ◽  
Calcium Buffer

ABSTRACTDiarrhea occurs in 2-50% of cases of COVID-19 (∼8% is average across series). The diarrhea does not appear to account for the disease mortality and its contribution to the morbidity has not been defined, even though it is a component of Long Covid or post-infectious aspects of the disease. Even less is known about the pathophysiologic mechanism of the diarrhea. To begin to understand the pathophysiology of COVID-19 diarrhea, we exposed human enteroid monolayers obtained from five healthy subjects and made from duodenum, jejunum, and proximal colon to live SARS-CoV-2 and virus like particles (VLPs) made from exosomes expressing SARS-CoV-2 structural proteins (Spike, Nucleocapsid, Membrane and Envelope). Results: 1) Live virus was exposed apically for 90 min, then washed out and studied 2 and 5 days later. SARS-Cov-2 was taken up by enteroids and live virus was present in lysates and in the apical>>basolateral media of polarized enteroids 48 h after exposure. This is the first demonstration of basolateral appearance of live virus after apical exposure. High vRNA concentration was detected in cell lysates and in the apical and basolateral media up to 5 days after exposure. 2) Two days after viral exposure, cytokine measurements of media showed significantly increased levels of IL-6, IL-8 and MCP-1. 3) Two days after viral exposure, mRNA levels of ACE2, NHE3 and DRA were reduced but there was no change in mRNA of CFTR. NHE3 protein was also decreased. 4) Live viral studies were mimicked by some studies with VLP exposure for 48 h. VLPs with Spike-D614G bound to the enteroid apical surface and was taken up; this resulted in decreased mRNA levels of ACE2, NHE3, DRA and CFTR. 4) VLP effects were determined on active anion secretion measured with the Ussing chamber/voltage clamp technique. S-D614G acutely exposed to apical surface of human ileal enteroids did not alter the short-circuit current (Isc). However, VLPS-D614G exposure to enteroids that were pretreated for ∼24 h with IL-6 plus IL-8 induced a concentration dependent increase in Isc indicating stimulated anion secretion, that was delayed in onset by ∼8 min. The anion secretion was inhibited by apical exposure to a specific calcium activated Cl channel (CaCC) inhibitor (AO1) but not by a specific CFTR inhibitor (BP027); was inhibited by basolateral exposure to the K channel inhibit clortimazole; and was prevented by pretreatment with the calcium buffer BAPTA-AM. 5) The calcium dependence of the VLP-induced increase in Isc was studied in Caco-2/BBe cells stably expressing the genetically encoded Ca2+ sensor GCaMP6s. 24 h pretreatment with IL-6/IL-8 did not alter intracellular Ca2+. However, in IL-6/IL-8 pretreated cells, VLP S-D614G caused appearance of Ca2+waves and an overall increase in intracellular Ca2+ with a delay of ∼10 min after VLP addition. We conclude that the diarrhea of COVID-19 appears to an example of a calcium dependent inflammatory diarrhea that involves both acutely stimulated Ca2+ dependent anion secretion (stimulated Isc) that involves CaCC and likely inhibition of neutral NaCl absorption (decreased NHE3 protein and mRNA and decreased DRA mRNA).

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