Early maternal separation induces alterations of colonic epithelial permeability and morphology

Li, Bo; Lee, Carol; Zani, Augusto; Zani‐Ruttenstock, Elke; Ip, Wan; Chi, Lijun; Olguin, Paul Delgado; Gonska, Tanja; Pierro, Agostino

doi:10.1007/s00383-014-3611-x

Cited by 14 publications

(17 citation statements)

References 22 publications

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“…Similar to what we have previously demonstrated6, MS induced morphological damage in the colon, but not in the ileum (Fig. 1A,B).…”

Section: Resultssupporting

confidence: 91%

“…Only colonic trans-cellular permeability increased in the MS group6 and the increase was inhibited by the administration of Antalarmin and Astressin, whereas Astressin-2β did not (Fig. 2Q).…”

Section: Resultsmentioning

confidence: 94%

“…This model has been used to study irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD) in adulthood23, as well as neonatal intestinal disorders456. Premature infants are separated from their mothers and commonly fed while in incubators.…”

mentioning

confidence: 99%

“…MS during the neonatal period in a mouse model can lead to significant intestinal epithelial dysfunction. We have previously shown that MS in neonatal mice changes the intestinal mucosal morphology, increases trans-cellular permeability and causes colonic inflammation456. In addition, changes in the microbiome are associated with MS-induced gut injury7.…”

mentioning

confidence: 99%

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Inhibition of corticotropin-releasing hormone receptor 1 and activation of receptor 2 protect against colonic injury and promote epithelium repair

Lee

Filler

et al. 2017

Sci Rep

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Maternal separation (MS) in neonates can lead to intestinal injury. MS in neonatal mice disrupts mucosal morphology, induces colonic inflammation and increases trans-cellular permeability. Several studies indicate that intestinal epithelial stem cells are capable of initiating gut repair in a variety of injury models but have not been reported in MS. The pathophysiology of MS-induced gut injury and subsequent repair remains unclear, but communication between the brain and gut contribute to MS-induced colonic injury. Corticotropin-releasing hormone (CRH) is one of the mediators involved in the brain–gut axis response to MS-induced damage. We investigated the roles of the CRH receptors, CRHR1 and CRHR2, in MS-induced intestinal injury and subsequent repair. To distinguish their specific roles in mucosal injury, we selectively blocked CRHR1 and CRHR2 with pharmacological antagonists. Our results show that in response to MS, CRHR1 mediates gut injury by promoting intestinal inflammation, increasing gut permeability, altering intestinal morphology, and modulating the intestinal microbiota. In contrast, CRHR2 activates intestinal stem cells and is important for gut repair. Thus, selectively blocking CRHR1 and promoting CRHR2 activity could prevent the development of intestinal injuries and enhance repair in the neonatal period when there is increased risk of intestinal injury such as necrotizing enterocolitis.

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“…Similar to what we have previously demonstrated6, MS induced morphological damage in the colon, but not in the ileum (Fig. 1A,B).…”

Section: Resultssupporting

confidence: 91%

Section: Resultsmentioning

confidence: 94%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Inhibition of corticotropin-releasing hormone receptor 1 and activation of receptor 2 protect against colonic injury and promote epithelium repair

Lee

Filler

et al. 2017

Sci Rep

Self Cite

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“…Another potentially important difference between preterm and term infants is that of maternal separation. Partial separation of mouse pups from the mother is enough to induce changes in colonic histology and permeability [37], although the relevance of these observations to NEC is unknown.…”

Section: Pathogenesismentioning

confidence: 99%

Current Research on the Epidemiology, Pathogenesis, and Management of Necrotizing Enterocolitis

2017

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Despite decades of research on necrotizing enterocolitis, we still do not fully understand the pathogenesis of the disease, or how to prevent or how to treat it. However, as a result of recent significant advances in the microbiology, molecular biology, and cell biology of the intestine of preterm infants and infants with necrotizing enterocolitis, there is some hope that research into this devastating disease will yield some important translation into effective prevention, more rapid diagnosis, and novel therapies.

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A spectrum of intestinal injury models in neonatal mice

Zani,

Zani-Ruttenstock,

Peyvandi

et al. 2015

Pediatr Surg Int

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Early maternal separation induces alterations of colonic epithelial permeability and morphology

Cited by 14 publications

References 22 publications

Inhibition of corticotropin-releasing hormone receptor 1 and activation of receptor 2 protect against colonic injury and promote epithelium repair

Inhibition of corticotropin-releasing hormone receptor 1 and activation of receptor 2 protect against colonic injury and promote epithelium repair

Current Research on the Epidemiology, Pathogenesis, and Management of Necrotizing Enterocolitis

A spectrum of intestinal injury models in neonatal mice

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