Variations in Cell and Structure Populations along the Length of Murine Small Intestine

Brennan, P.C.; McCullough, Jeffrey S.; Carr, K. E.

doi:10.1159/000016662

Cited by 5 publications

(6 citation statements)

References 19 publications

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“…In addition, regeneration after the de struction of mucosal integrity by prolonged preserva tion and transplantation was more pronounced in the jejunum than in the ileum (13). The reason why the proximal small intestine was more fragile than the dis tal small intestine in the present Ussing chamber exper iment is not clear, but could be related to the fact that the fragile villous region is taller in the proximal small intestine than in the distal one (14).…”

Section: Discussionmentioning

confidence: 57%

Segmental Difference of Mucosal Damage along the Length of a Mouse Small Intestine in an Ussing Chamber

Inagaki

Natori

Ohgishi

et al. 2005

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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SummaryThe Ussing chamber is often used for in vitro investigations into the transport physiology of epithelia including the small intestine. However, the morphological and func tional integrity of the small intestine incubated in an Ussing chamber has been largely ignored. The present study attempted to compare the mucosal injury among different seg ments of the mouse small intestine when incubated in an Ussing chamber. To assess the functional damage, we measured changes in the transmural potential difference (PD) evoked by adding glucose to the mucosal solution and forskolin to the mucosal and serosal solutions. Morphological deterioration was assessed histologically. The villi in the duode num and proximal jejunum were morphologically damaged by 2h of incubation in an Ussing chamber and almost completely destroyed within 4h, while crypts remained intact. The villi were moderately damaged in the distal jejunum. In contrast, the integrity of the villi and crypts was maintained in the ileum for 4h. The basal PD and forskolin-induced PD were maintained up to 4h of incubation in all segments. On the other hand, the glucose induced PD was not apparent in the duodenum at 0h, and was gradually suppressed to zero in the proximal jejunum by 4h, although the glucose-induced PD was maintained for 4h in the ileum. The loss of villous epithelial integrity was correlated with the disappearance of the glucose-induced PD, while both the basal and forskolin-induced PD were retained, even in the tissue with disrupted villi. It is concluded that the mucosa of the proximal small intes tine was rapidly injured in the Ussing chamber, particularly in the villi, while the integrity of the mucosa of the distal small intestine was maintained for 4h. The glucose-induced PD, but not the basal or forskolin-induced PD, can be used as a marker of the villous integrity.

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Section: Discussionmentioning

confidence: 57%

Segmental Difference of Mucosal Damage along the Length of a Mouse Small Intestine in an Ussing Chamber

Inagaki

Natori

Ohgishi

et al. 2005

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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“…The thickness of the total rat duodenum mucous layer is ϳ170 m, while that of the ileum is 476 m (4). Also, when this mucosal layer is removed by suction, the ileum replaces mucus at a faster rate than the duodenum (9). With a decreased thickness and reduced rate of mucous restoration, the duodenum faces disadvantages to buffer itself against luminal contents.…”

Section: B Heat Strokementioning

confidence: 99%

Regional susceptibility to stress-induced intestinal injury in the mouse

Novosad

Richards

Phillips

et al. 2013

American Journal of Physiology-Gastrointestinal and Liver Physi

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Injury to the intestinal mucosa is a life-threatening problem in a variety of clinical disorders, including hemorrhagic shock, trauma, burn, pancreatitis, and heat stroke. The susceptibility to injury of different regions of intestine in these disorders is not well understood. We compared histological injury across the small intestine in two in vivo mouse models of injury, hemorrhagic shock (30% loss of blood volume) and heat stroke (peak core temperature 42.4°C). In both injury models, areas near the duodenum showed significantly greater mucosal injury and reductions in villus height. To determine if these effects were dependent on circulating factors, experiments were performed on isolated intestinal segments to test for permeability to 4-kDa FITC-dextran. The segments were exposed to hyperthermia (42°C for 90 min), moderate simulated ischemia (Po2 ∼30 Torr, Pco2 ∼60 Torr, pH 7.1), severe ischemia (Po2 ∼20 Torr, Pco2 ∼80 Torr, pH 6.9), or severe hypoxia (Po2 ∼0 Torr, Pco2 ∼35 Torr) for 90 min, and each group was compared with sham controls. All treatments resulted in marked elevations in permeability within segments near the duodenum. In severe hypoxia or hyperthermia, permeability was also moderately elevated in the jejunum and ileum; in moderate or severe ischemia, permeability was unaffected in these regions. The results demonstrate increased susceptibility of proximal regions of the small intestine to acute stress-induced damage, irrespective of circulating factors. The predominant injury in the duodenum may impact the pattern of acute inflammatory responses arising from breach of the intestinal barrier, and such knowledge may be useful for designing therapeutic strategies.

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“…In mice, a-defensins are exclusively expressed in Paneth cells (PCs), which are epithelial cells located in the crypts of Lieberkhün lining the small intestine (3). PCs are heterogeneously distributed in the small intestine with a higher frequency in the ileum compared with those in the duodenum and jejunum (4).…”

mentioning

confidence: 99%

TLR9-Dependent Induction of Intestinal α-Defensins by Toxoplasma gondii

Foureau

Mielcarz

Ménard

et al. 2010

The Journal of Immunology

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α-Defensins (or Cryptdins [Crps]) are a group of antimicrobial peptides produced as a component of Paneth cell (PC) secretory granules in the small intestine. In vivo ligation of TLR9 by synthetic agonists leads to PC degranulation, although the mechanism by which this occurs remains uncertain. In this report, we investigated TLR9-dependent mechanisms, triggered by the parasite Toxoplasma gondii, inducing Crp release in the lumen. Oral challenge of C57BL/6J (B6) wild-type (WT) mice with T. gondii induced TLR9 mRNA upregulation associated with a marked increase of type I IFN mRNA expression. PC secretory granules were released, and Crp-3/-5 mRNA expression by purified epithelial cells was increased following oral challenge of B6 WT mice. Although PCs failed to degranulate in infected B6 TLR9−/− mice, i.p. injection of mouse IFN-β alone led to Crp-3/-5 mRNA upregulation in B6 WT and TLR9−/− mice. In addition, modulation of Crp mRNA expression in response to T. gondii infection was abrogated in B6 IFNAR−/− mice, which lack a functional type I IFN receptor. Taken together, these data demonstrate that T. gondii induces Crp-3/-5 production and release by PCs via a TLR9-dependent production of type I IFNs. Crps have a limited direct effect against T. gondii but may indirectly affect the early control of T. gondii invasiveness by promoting the initiation of a protective Th1 response against the parasite.

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Variations in Cell and Structure Populations along the Length of Murine Small Intestine

Cited by 5 publications

References 19 publications

Segmental Difference of Mucosal Damage along the Length of a Mouse Small Intestine in an Ussing Chamber

Segmental Difference of Mucosal Damage along the Length of a Mouse Small Intestine in an Ussing Chamber

Regional susceptibility to stress-induced intestinal injury in the mouse

TLR9-Dependent Induction of Intestinal α-Defensins by Toxoplasma gondii

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