Epidemiology of Inflammatory Bowel Disease

Ekbom, Anders

doi:10.1159/000061792

Cited by 7 publications

(2 citation statements)

References 21 publications

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“…First, there is a peak of diagnosis between 15 and 35 for both CD and UC. There is also a later peak, particularly for CD, between 65 and 74 years of age that is more prominent than described in many studies 28–31. However, the number of patients in these age groups is small, as reflected by the wide 95% CIs.…”

Section: Discussionmentioning

confidence: 76%

High incidence of Crohnʼs disease in Canterbury, New Zealand: Results of an epidemiologic study

Gearry¹,

Richardson²,

Frampton³

et al. 2006

Inflammatory Bowel Diseases

227

193

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Section: Discussionmentioning

confidence: 76%

High incidence of Crohnʼs disease in Canterbury, New Zealand: Results of an epidemiologic study

Gearry¹,

Richardson²,

Frampton³

et al. 2006

Inflammatory Bowel Diseases

227

193

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“…Destruction of the intestinal epithelium fence is observed in inflammatory bowel disease (IBD; Ekbom, 1999; Tanimoto et al., 2020), which is involved in the immoderate production of oxidant species, pro‐inflammatory signals released from enterocytic and immune cells, leading to serious mucosa injury by sustained and increasing inflammation. The intestinal barrier is critical to the health and is one of the most metabolically dynamic systems in the body, and the integrity of its epithelial monolayer is vital to maintain host homeostasis because it inhibits the invasion of luminal antigens (Nishitani et al., 2013).…”

Section: Introductionmentioning

confidence: 99%

Acai berry extract as a regulator of intestinal inflammation pathways in a Caco‐2 and RAW 264.7 co‐culture model

Kim

Jin

et al. 2021

J Food Biochem

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The aim of this study was to assess the anti‐inflammatory effects of acai berries in a Caco‐2 and RAW 264.7 macrophage co‐culture model. The acai berry extract (ABE) was prepared using 70% ethanol, and total anthocyanin, polyphenol, and flavonoid contents in ABE were analyzed. To the antioxidant activity of ABE, we measured radical scavenging activity as well as ferric reducing antioxidant power values. Prior to inducing inflammation, Caco‐2 cells were co‐cultured with RAW 264.7. Inflammation was induced using lipopolysaccharides (LPS) in RAW 264.7 cells. The transepithelial electrical resistance value was significantly recovered and the mRNA level of tight junction proteins, including ZO‐1, JAM‐1, and claudin‐4, tended to increase compared with that in the LPS group. LPS‐induced interleukin (IL)‐6, IL‐8, and prostaglandin E2 levels reduced significantly following treatment with the highest ABE concentration. In the highest ABE concentration, the phosphorylation of p65, p38 mitogen‐activated protein kinase, and c‐Jun N‐terminal kinase was downregulated compared with the LPS group. The phosphorylation of extracellular signal‐regulated kinase showed a decreased tendency. These results suggest that acai berry may improve gastrointestinal health. Practical applications Acai berry is known to have abundant anthocyanin, which has many biological activities, including anti‐inflammatory, antioxidant, antihypertensive, and anticytotoxic/cytoprotective activities. This study demonstrated the anti‐inflammatory effects of acai berry extracts via TEER value, expression of tight junction protein, and production of inflammatory mediators and cytokines in the Caco‐2 and RAW 264.7 co‐culture model. Therefore, acai berry has the potential to prevent intestinal inflammatory diseases.

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State-of-the Art Lecture: The multifactorial pathogenesis of inflammatory bowel disease

Fiocchi¹

Falk Symposium

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Epidemiology of Inflammatory Bowel Disease

Cited by 7 publications

References 21 publications

High incidence of Crohnʼs disease in Canterbury, New Zealand: Results of an epidemiologic study

High incidence of Crohnʼs disease in Canterbury, New Zealand: Results of an epidemiologic study

Acai berry extract as a regulator of intestinal inflammation pathways in a Caco‐2 and RAW 264.7 co‐culture model

State-of-the Art Lecture: The multifactorial pathogenesis of inflammatory bowel disease

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