VIP enhances colonic crypt function at baseline.

<p>Exogenous VIP was administered to VIPKO mice (VIPKO-VIP) daily for 10 days. Immunostaining for Ki67 and quantitative analysis of Ki67+ve cells (A). Immunostaining for BrdU+ve cells and calculated spatial distribution at 72h post injection (B). Quantitative analysis of TUNEL +ve crypt IEC (C). Epithelial permeability measured by FITC dextran (D); n = 6–10 animals/group, results are represented as means ± SEM, *P<0.05, **P< 0.01, ***P<0.001. Scale bar = 50 μm.</p

Real time PCR analysis of genes in wild type and VIPKO mice.

<p>Real time PCR analysis of genes in wild type and VIPKO mice.</p

VIPKO mice exhibit increased susceptibly to chemically induced DNBS- colitis.

<p>At day 3 post-DNBS treatment VIPKO mice display shrunken ceca and significant thickening/damage of the mid to distal colon with fat wrapping when compared to WT mice (A), with significantly increased macroscopic damage scores (B). Representative H&E staining of Day 3 post-DNBS treated WT and VIPKO mice (C), when scored histologically (D) shows a significant increase in overall damage in VIPKO tissues compared to WT. Water content of luminal stool expressed as the percentage of the initial stool weight lost after drying at 37°C for 48h (E); n = 6–9 animals/group, results are represented as means ± SEM, *P<0.05, **P<0.01.</p

VIP regulates colonic goblet cell numbers and function at baseline.

<p>Exogenous VIP was administered to VIPKO mice (VIPKO-VIP) daily for 10 days. Selective labeling of neutral mucins with PAS and quantification of PAS+ve cells as a percentage of total IEC/crypt (A). Immunostaining and quantitative analysis of colonic Muc2+ve cells (B) and Tff3 +ve cells (C). Relative expression of colonic Muc2 and Tff3 (D), and Cdx1 and Cdx2 (E); n = 4–6 animals/group, results are represented as means ± SEM, *P<0.05, **P< 0.01, ***P<0.001. Scale bar = 50 μm. Arrows highlight cells that are positive in PAS staining (A), Muc2 staining (B) and Tff3 staining (C).</p

VIPKO mice display aberrant crypt structure at baseline.

<p>Representative H&E stained colon sections and quantitative analysis of crypt height and width in WT and VIPKO mice. n = 6–10 animals/ group, results are represented as means ± SEM, *P<0.05, ***P<0.001.</p

Past and future burden of inflammatory bowel diseases based on modeling of population-based data

BACKGROUND & AIMS: Inflammatory bowel diseases (IBDs) exist worldwide, with high prevalence in North America. IBD is complex and costly, and its increasing prevalence places a greater stress on health care systems. We aimed to determine the past current, and future prevalences of IBD in Canada. METHODS: We performed a retrospective cohort study using population-based health administrative data from Alberta (2002–2015), British Columbia (1997– 2014), Manitoba (1990–2013), Nova Scotia (1996–2009), Ontario (1999–2014), Quebec (2001–2008), and Saskatchewan (1998–2016). Autoregressive integrated moving average regression was applied, and prevalence, with 95% prediction intervals (PIs), was forecasted to 2030. Average annual percentage change, with 95% confidence intervals, was assessed with log binomial regression. RESULTS: In 2018, the prevalence of IBD in Canada was estimated at 725 per 100,000 (95% PI 716–735) and annual average percent change was estimated at 2.86% (95% confidence interval 2.80%–2.92%). The prevalence in 2030 was forecasted to be 981 per 100,000 (95% PI 963–999): 159 per 100,000 (95% PI 133–185) in children, 1118 per 100,000 (95% PI 1069–1168) in adults, and 1370 per 100,000 (95% PI 1312–1429) in the elderly. In 2018, 267,983 Canadians (95% PI 264,579–271,387) were estimated to be living with IBD, which was forecasted to increase to 402,853 (95% PI 395,466–410,240) by 2030. CONCLUSION: Forecasting prevalence will allow health policy makers to develop policy that is necessary to address the challenges faced by health systems in providing high-quality and cost-effective care