200 Molecular Mechanism of IL-1β-Induced Increase in CACO-2 Intestinal Epithelial Tight Junction Permeability

Al–Sadi, Rana; Ye, Dongmei; Ma, Thomas Y.

doi:10.1016/s0016-5085(08)60169-9

Cited by 1 publication

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“…Obesity has been implicated to increase intestinal permeability in animal models 6–9 . Epithelial tight junctions that maintain epithelial integrity can be damaged by circulating proinflammatory cytokines released from visceral abdominal fat in centrally obese individuals 10 , 11 .…”

Section: Introductionmentioning

confidence: 99%

“…Obesity has been implicated to increase intestinal permeability in animal models. [6][7][8][9] Epithelial tight junctions that maintain epithelial integrity can be damaged by circulating proinflammatory cytokines released from visceral abdominal fat in centrally obese individuals. 10,11 In addition, GER has been shown to lead to esophageal epithelial barrier damage characterized by dilated intercellular spaces (DIS) in the squamous epithelium.…”

Section: Introductionmentioning

confidence: 99%

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Influence of reflux and central obesity on intercellular space diameter of esophageal squamous epithelium

et al. 2016

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Background: While central obesity increases gastroesophageal reflux (GER) by mechanically disrupting the anti-reflux barrier, limited data exist on pathways by which central obesity may potentiate esophageal injury by non-mechanical means. Obesity has been associated with an impaired epithelial intestinal barrier. Objective: We aimed to assess the influence of central obesity and reflux on the squamous esophageal epithelial intercellular space diameter (ICSD). Methods: The ICSD was measured using electron microscopy in esophageal biopsies from individuals who underwent ambulatory pH monitoring and endoscopy. Anthropometric measurements were obtained on all participants. Participants were classified into four groups: with and without central obesity and reflux. Results: Sixteen individuals were studied with four in each study group. The mean ICSD was almost three-fold greater (p < 0.001) in the group with central obesity without reflux, compared to controls without central obesity and reflux. It was also comparable to the ICSD in groups with acid reflux only and those with both reflux and central obesity. Conclusions: There is evidence of esophageal squamous ICSD increase in individuals with central obesity who do not have evidence of acid and nonacid reflux on ambulatory pH monitoring. This may reflect a mechanism by which central obesity potentiates reflux-induced esophageal injury and inflammation.

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Section: Introductionmentioning

confidence: 99%