Lack of evidence <i>in vivo</i> for a remote effect of <i>Escherichia coli</i> heat stable enterotoxin on jejunal fluid absorption

Lucas, Michael L.; Duncan, Niall W.; O’reilly, N. F.; McIlvenny, TJ; Nelson, Y. B.

doi:10.1111/j.1365-2982.2007.01046.x

Cited by 8 publications

(8 citation statements)

References 16 publications

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“…[40][41][42] STa-mediated secretion may also involve local reflex arcs in the enteric nervous system (ENS); however, it does not involve the autonomic nervous system. 43 Most of the support for this idea comes from studies that inhibit the ENS and subsequently reduce the secretory effect of STa. [44][45][46] The neurotransmitters critical in these responses are nitric oxide (NO) and VIP, 40,46 whereas PGE 2 and 5-HT are not involved.…”

Section: Heat Stable Toxin-mediated Secretory Diarrheamentioning

confidence: 99%

Pathophysiology of Diarrhea in Calves

Foster

Smith

2009

Veterinary Clinics of North America: Food Animal Practice

278

269

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Infectious diarrhea in calves is most commonly associated with enterotoxigenic Escherichia coli, Cryptosporidium parvum, rotavirus, coronavirus, or some combination of these pathogens. Each of these agents leads to diarrhea through either secretion or malabsorption/maldigestion, though the specific mechanisms and pathways may differ. Specific pharmacologic control and treatment are dependent on gaining a greater understanding of the pathophysiology of these organisms.

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Section: Heat Stable Toxin-mediated Secretory Diarrheamentioning

confidence: 99%

Pathophysiology of Diarrhea in Calves

Foster

Smith

2009

Veterinary Clinics of North America: Food Animal Practice

278

269

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“…For example, Moxley and co-workers utilized isogenic strains of ETEC to address the role of STb and other virulence factors in gnotobiotic piglets [22], while Lucas et al,[23] recently addressed the role of STa in the elicitation of distanced effects on fluid absorption in the intestine of rats.…”

Section: Heat Stable Enterotoxinsmentioning

confidence: 99%

Toxins from bacteria

Henkel

Baldwin

Barbieri

2010

Experientia Supplementum

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Bacterial toxins damage the host at the site of bacterial infection or distanced from the site of infections. Bacterial toxins can be single proteins or organized as oligomeric protein complexes and are organized with distinct AB structure-function properties. The A domain encodes a catalytic activity; ADP-ribosylation of host proteins is the earliest post-translational modification determine to be performed by bacterial toxin, and now include glucosylation and proteolysis among other s. Bacterial toxins also catalyze the non-covalent modification of host protein function or can modify host cell properties through direct protein-protein interactions. The B domain includes two functional domains: a receptor-binding domain, which defines the tropism of a toxin for a cell and a translocation domain that delivers A domain across a lipid bilayer, either on the plasma membrane or the endosome. Bacterial toxins are often characterized based upon the section mechanism that delivers the toxin out of the bacterium, termed type I–VII. This review will overview the major families of bacterial toxins and will also describe the specific structure-function properties of the botulinum neurotoxins.

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“…; Rolfe and Levin ; Lucas et al. , , ). As there are disparities in terms of Cl − ion secretion, latency of action and the amount of net fluid secretion between two major effectors of secretory diarrhea, viz .…”

Section: Introductionmentioning

confidence: 99%

An investigation into the relationship between small intestinal fluid secretion and systemic arterial blood pressure in the anesthetized rat

Lucas

Morrison

2015

Physiol Rep

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The effects of changes in the steady level of diastolic blood pressure on fluid flux across the jejunum has been investigated in the anesthetized rat during perfusion with a nutrient-free and Na+-free solution. Diastolic blood pressure was manipulated by intravenous infusions, during the jejunal perfusions, of vasodilators (vasoactive intestinal polypeptide, acetyl-β-methylcholine, and phentolamine) and a vasoconstrictor (arginine vasopressin), each of which acts through a different cellular mechanism. The outcome was that fluid flux was related by a parabolic relationship with diastolic blood pressure in which net secretion occurred over the range 40–100 mmHg, whereas net absorption was recorded at diastolic pressures exceeding 100 mmHg and below 40 mmHg. Against a background of normal absorption promoted by perfusion with 145 mmol L−1 Na+/5 mmol L−1 glucose solution, reductions in diastolic blood pressure markedly reduced the mean rate of fluid absorption by 58% overall, whereas the rate of glucose absorption remained unchanged. Our results were explained on the basis that vasodilatation led to increased capillary pressure and then to net filtration of fluid from the mesenteric capillary bed. Experiments in which Escherichia coli heat-stable toxin was added to the jejunal perfusate confirmed the absence of a secretory response, which was consistent with the absence of effect of the toxin on diastolic blood pressure.

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Lack of evidence in vivo for a remote effect of Escherichia coli heat stable enterotoxin on jejunal fluid absorption

Cited by 8 publications

References 16 publications

Pathophysiology of Diarrhea in Calves

Pathophysiology of Diarrhea in Calves

Toxins from bacteria

An investigation into the relationship between small intestinal fluid secretion and systemic arterial blood pressure in the anesthetized rat

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