Fibrocytes are recruited early in the inflammatory phase and likely differentiate into fibroblasts/myofibroblasts until the fibrosis phase. They may enhance inflammation by producing TNF-α and can directly augment fibrosis by producing ColI.

BACKGROUND/OBJECTIVES: A significant proportion of Crohn's disease (CD) patients receiving infliximab (IFX) maintenance therapy show loss of responsiveness despite a good initial response. The factors other than immunomodulators that prevent IFX dose escalation have yet to be fully elucidated. This study was performed to identify clinical factors or concomitant therapies associated with sustained response to IFX. SUBJECTS/METHODS: Seventy-four consecutive CD patients who had successful IFX induction therapy between 2002 and 2010 underwent IFX maintenance therapy. Patients showing loss of response to IFX were treated with IFX intensification therapy. Factors involved in the sustained response to IFX were investigated retrospectively. RESULTS: After a median follow-up of 85 weeks, loss of response to IFX was observed in 30 (40.5%) cases. On logistic regression analysis, concomitant use of enteral nutrition (EN) therapy (elemental and/or polymeric formulas) was identified as an independent factor associated with sustained response to IFX. Receiver operating characteristic curve analysis indicated a cutoff value of 600 kcal/day. We divided the patients into the 'EN group' (X600 kcal/day) and 'control group' (o600 kcal/day). The cumulative number of loss of response was significantly lower in the EN group (odds ratio: 0.23, P ¼ 0.0043). Kaplan-Meier analysis confirmed the significantly lower rate of loss of response in the EN group (P ¼ 0.013). Multivariate hazard ratio was 0.37 (P ¼ 0.025). Type of EN formula did not affect the results. CONCLUSIONS: Concomitant use of EN X600 kcal/day is likely to yield a sustained response to IFX in CD patients.

SUMMARY BackgroundWhen treating patients with severe ulcerative colitis (UC), accurate prediction of drug efficacy contributes to early clinical decision-making.

This is the first study indicating that intestinal epithelial cells with impaired autophagy lose their adhesive capacity in the presence of TNF-α. These observations indicate that impairment of autophagy leads to disruption of the intestinal epithelial cell layers in TNF-α-rich environments.

Expression of Shh was correlated with the speed of gastric ulcer healing, promoting the regeneration of gastric mucosa.