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Background Crohn’s disease (CD), ulcerative colitis (UC), and indeterminate colitis are inflammatory bowel diseases (IBDs) that adversely affect the healthcare needs and quality of life (QoL) of people with IBD. The aim of this study was to explore the needs and perceptions of people with IBD in a primary care setting. Methods This sequential explanatory mixed-methods study consisted of a cross-sectional survey (included validated tools), followed by semistructured interviews on participants’ perceptions: IBD management, healthcare professionals, IBD care, flare management, and pharmacist’s IBD roles. Results Sixty-seven participants completed the survey, and 8 completed interviews. Quantitative findings: Age at diagnosis had significant association with medication nonadherence (P = .04), QoL (P = .04), and disease control (P = .01) among the respondents. The odds of medication nonadherence were 8 times (adjusted odds ratio [AOR] = 8.04, 95% confidence interval [CI] = 1.08, 60.10) higher among younger participants aged Conclusions Primary healthcare professionals are well positioned but need targeted training to influence the needs of IBD patients. The specialty role of an IBD educator could complement existing services to deliver and address patient-specific care.

Inflammatory bowel disease is associated with a number of comorbidities that arise at extraintestinal sites, including the lung. Pulmonary manifestations reported in inflammatory bowel disease include bronchiectasis, chronic bronchitis and importantly, a range of subclinical respiratory abnormalities that are often overlooked in routine clinical evaluation. Whereas evidence for the pulmonary manifestations of Inflammatory bowel disease is increasing, little is known about the immunologic and physiologic mechanisms regulating cross-talk between the gut and lung during disease. This review examines reported lung involvement in Inflammatory bowel disease and discusses the possible immune pathways that underlie pulmonary pathologies. These mechanisms include dysfunctional immune-cell homing, systemic inflammation, and microbial dysbiosis; all of which may contribute to Inflammatory bowel disease-induced pulmonary inflammation. These mechanisms are discussed in the context of our current knowledge of the shared mucosal immune system and the immunology of Inflammatory bowel disease.

Pharmacological induction of hypoxia-inducible factor (HIF), a global transcriptional regulator of the hypoxic response, by prolyl hydroxylase inhibitors (PHDi) is protective in murine models of colitis, and epithelial cells are critical for the observed therapeutic efficacy. Because systemic HIF activation may lead to potentially negative off-target effects, we hypothesized that targeting epithelial HIF through oral delivery of PHDi would be sufficient to protect against colitis in a mouse model.Using a chemically induced trinitrobenzene sulfonic acid murine model of colitis, we compared the efficacy of oral and intraperitoneal (i.p.) delivery of the PHDi; AKB-4924 in preventing colitis, as measured by endoscopy, histology, barrier integrity, and immune profiling. Furthermore, we measured potential off-target effects, examining HIF and HIF target genes in the heart and kidney, as well as erythropoietin and hematocrit levels.Oral administration of AKB-4924 exhibited mucosal protection comparable i.p. dosing. Oral delivery of PHDi led to reduced colonic epithelial HIF stabilization compared with i.p. delivery, but this was still sufficient to induce transcription of downstream HIF targets. Furthermore, oral delivery of PHDi led to reduced stabilization of HIF and activation of HIF targets in extraintestinal organs.Oral delivery of PHDi therapies to this intestinal mucosa protects against colitis in animal models and represents a potential therapeutic strategy for inflammatory bowel disease, which also precludes unwanted extraintestinal effects.

BACKGROUND Abdominal pain frequently accompanies inflammatory disorders of the gastrointestinal tract (GIT), and animal models of GIT inflammation have been developed to explore the role of the central nervous system (CNS) in this process. Here, we summarize the evidence from animal studies for CNS plasticity following GIT inflammation. METHODS A systematic review was conducted to identify studies that: (1) used inflammation of GIT organs, (2) assessed pain or visceral hypersensitivity, and (3) presented evidence of CNS involvement. Two hundred and eight articles were identified, and 79 were eligible for analysis. RESULTS Rats were most widely used (76%). Most studies used adult animals (42%) with a bias toward males (74%). Colitis was the most frequently used model (78%) and 2,4,6-trinitrobenzenesulfonic acid the preferred inflammatory agent (33%). Behavioral (58%), anatomical/molecular (44%), and physiological (24%) approaches were used alone or in combination to assess CNS involvement during or after GIT inflammation. Measurement times varied widely ( 2 wk after inflammation). Blinded outcomes were used in 42% studies, randomization in 10%, and evidence of visceral inflammation in 54%. Only 3 studies fulfilled our criteria for high methodological quality, and no study reported sample size calculations. CONCLUSIONS The included studies provide strong evidence for CNS plasticity following GIT inflammation, specifically in the spinal cord dorsal horn. This evidence includes altered visceromotor responses and indices of referred pain, elevated neural activation and peptide content, and increased neuronal excitability. This evidence supports continued use of this approach for preclinical studies; however, there is substantial scope to improve study design.

Resolvin-E1 (RvE1) has been demonstrated to promote inflammatory resolution in numerous disease models. Given the importance of epithelial cells to coordination of mucosal inflammation, we hypothesized that RvE1 elicits an epithelial resolution signature. Initial studies revealed that the RvE1-receptor (ChemR23) is expressed on intestinal epithelial cells (IECs) and that microarray profiling of cells exposed to RvE1 revealed regulation of inflammatory response gene expression. Notably, RvE1 induced intestinal alkaline phosphatase (ALPI) expression and significantly enhanced epithelial ALPI enzyme activity. One role recently attributed to ALPI is the detoxification of bacterial LPS. In our studies, RvE1-exposed epithelia detoxified LPS (assessed by attenuation of NF-κB signaling). Furthermore, in epithelial-bacterial interaction assays, we determined that ALPI retarded the growth of Escherichia coli . To define these features in vivo, we used a murine dextran sulfate sodium (DSS) model of colitis. Compared with vehicle controls, administration of RvE1 resulted in significant improvement of disease activity indices (e.g., body weight, colon length) concomitant with increased ALPI expression in the intestinal epithelium. Moreover, inhibition of ALPI activity resulted in increased severity of colitis in DSS-treated animals and partially abrogated the protective influence of RvE1. Together, these data implicate a previously unappreciated role for ALPI in RvE1-mediated inflammatory resolution.