Small intestinal permeability. 1. Effects of ischaemia and exposure to acetyl salicylate.

Kingham, J. G. C.; Whorwell, P J; Loehry, C A

doi:10.1136/gut.17.5.354

Cited by 37 publications

(6 citation statements)

References 20 publications

(20 reference statements)

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“…The process employs an endocytic mechanism (6,41), is energy dependent, and has been shown to be inhibited by compounds which inhibit glycolysis or oxidative phosphorylation (6). Numerous studies with macromolecules such as horseradish peroxidase, polyvinylpyrrolidone, insulin, and vitamin B12 have confirmed this finding (6,16,19,21,28,32,41). Our data support this hypothesis.…”

Section: Discussionmentioning

confidence: 77%

In vitro interaction of Mycobacterium avium with intestinal epithelial cells

Mapother¹,

Songer²

1984

Infect Immun

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Human intestinal epithelial cell monolayers were inoculated with cultures of Mycobacterium avium serotype 2, 8, or 10 that were viable, autoclaved, Formalin killed, exposed to UV light, or suspended in anti-M. avium serotype 2 serum. The effects of four reagents known to block phagocytosis or endocytosis (cytochalasin B, dibutyryl cyclic adenosine monophosphate, iodoacetate, and 2,4-dinitrophenol) on the bacteria-cell interaction were also studied. The maximum uptake of pathogenic M. avium by human intestinal epithelial cells occurred after 2 to 3 h of incubation. Serotype 2 was taken up in greater quantity than serotype 8 or 10. Saprophytic mycobacteria did not attach to or penetrate the host cells. The data showed that viable mycobacteria are ingested by host cells, whereas dead organisms are not. Components of the bacterial cells are partially, but not solely, responsible for the phagocytosis of M. avium serotype 2 by human intestinal epithelial cells. Furthermore, uptake of M. avium by human intestinal epithelial cells was suppressed by reagents which inhibit uptake by known phagocytic cells, suggesting that the mechanism of uptake is an endocytic process induced by virulent mycobacteria.

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Section: Discussionmentioning

confidence: 77%

In vitro interaction of Mycobacterium avium with intestinal epithelial cells

Mapother¹,

Songer²

1984

Infect Immun

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“…Finally, the study of Kingham et al [20] should be mentioned. These authors used an approach similar to ours, viz., perfusion of the intestine following ischaemia or after chemical destruction of the villus crests, to examine the changes in mucosal permeability resulting from epithelial destruction.…”

Section: Discussionmentioning

confidence: 98%

“…In view of the complication imposed by the vascular stasis referred to above, we have also attempted to induce similar morphological and functional changes in the epithelial layer by chemical means to obtain further information on the source of secretion following disruption of the villus epithelium. Although the local application of corrosive substances, such as acids [11,17,28], formalin [35], or concentrated solutions of polymers [4], has been used previously to explore the regenerative potential of the intestinal mucosa, only three attempts seem to have been made to destroy selectively one part of the intestinal mucosa by chemical means: Roggin et al [33] and Browning et al [1] damaged the tips of the villi by the introduction into the ileum of very hypertonic solutions of sodium sulphate, to which the crypts were apparently refractory, and Kingham et al [20] used unionised acetyl-salicylate to obtain analogous effects. In the present study, we have ostensibly achieved the same results by exposure of the dog ileal mucosa in vivo to a solution of Triton X-100.…”

Section: Discussionmentioning

confidence: 99%

Source of net water and electrolyte loss following intestinal ischaemia

1980

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Ischaemia of the dog intestine lasting 1 h causes desquamation of the epithelium at the villus tips and congestion in the villus capillaries. The crypt cells are relatively undamaged. These changes are associated with a loss of active transport of organic solutes, determined in vitro, a reduction in mucosal sucrase activity and an abolition of glucose absorption in vivo. A profuse net loss of water and electrolytes into the lumen in vivo develops. The net sodium loss is due primarily to an inhibition of the lumen-blood flux of this ion, the blood-lumen flux being relatively unchanged. In uraemic dogs, the loss of urea into the lumen is the same in control and ischaemic loops, testifying to the lack of change in the unidirectional water flow from blood to lumen. Perfusion of the dog intestine with 1% Triton X-100 leads to morphological changes that have certain similarities with those provoked by ischaemia. Damage was restricted to the villus tips, protection from further alterations apparently being provided by a mucus layer that forms on the mucosal surface; the crypt region remained unchanged. After 10 min exposure, organic solute transport in vitro and glucose absorption in vivo were both reduced by not abolished; sodium and water absorption in vivo were suppressed, but no net secretion occurred. To account for these observations, we have suggested that the normal crypt cell is a secretory element with respect to sodium and water. During maturation, its absorptive properties develop such that the mature enterocyte, possessing both absorptive and secretory mechanisms, is capable of net absorption of sodium. After destruction of the villus tips, net secretion continues in the crypts; if there are insufficient villus cells remaining to ensure reabsorption, a net secretory capacity is observed.

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“…29,30,a Clearance of radiolabeled albumin from blood to the intestinal lumen has been used as a marker of early mucosal injury. [31][32][33][34][35] Injury leading to an increase in mucosal permeability would result in an increase in clearance rate. Albumin concentrations (in the nanogram range) in blood, urine, peritoneal fluid, and luminal contents have been measured by use of radioimmunoassay, immunoagglutination assay, and ELISA.…”

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confidence: 99%