Inflammatory bowel disease (IBD) is characterized by chronic intestinal inflammation that includes Crohn´s disease (CD) and ulcerative colitis (UC). Although the etiology is still unknown, some specific factors have been directly related to IBD, including genetic factors, abnormal intestinal immunity, and/or gut microbiota modifications. Recent findings highlight the primary role of the gut microbiota closely associated with a persistent inappropriate inflammatory response. This gut environment of dysbiosis in a susceptible IBD host can increasingly worsen and lead to colonization and infection with some opportunistic pathogens, especially Clostridium difficile. C. difficile is an intestinal pathogen considered the main cause of antibiotic-associated diarrhea and colitis and an important complication of IBD, which can trigger or worsen an IBD flare. Recent findings have highlighted the loss of bacterial cooperation in the gut ecosystem, as well as the pronounced intestinal dysbiosis, in patients suffering from IBD and concomitant C. difficile infection (CDI). The results of intestinal microbiota studies are still limited and often difficult to compare because of the variety of disease conditions. However, these data provide important clues regarding the main modifications and interrelations in the complicated gut ecosystem to better understand both diseases and to take advantage of the development of new therapeutic strategies. In this review, we analyze in depth the gut microbiota changes associated with both forms of IBD and CDI and their similarity with the dysbiosis that occurs in CDI. We also discuss the metabolic pathways that favor the proliferation or decrease in several important taxa directly related to the disease.

Objective: Many acute coronary syndrome (ACS) patients are nonadherent to cardiovascular medications despite their known benefits for lowering risk of recurrent cardiovascular events. Research suggests that greater cardiac-related fear of recurrence (FoR) may be associated with higher nonadherence to cardiovascular medications and avoidance of physical activity. We aim to test the effect of an intervention that targets FoR as a potentially modifiable mechanism underlying nonadherence to recommended health behaviors among patients with suspected ACS. Method: The INFORM trial ("INvestigating Fear Of Recurrence as a modifiable Mechanism of behavior change to improve medication adherence in acute coronary syndrome patients") is a double-blind, parallel-group randomized clinical trial. It compares an 8-session, at-home, electronic tablet-delivered, cognitive bias modification training (CBMT) intervention with a sham control. Patients who experience high perceived threat at the time of presentation to the emergency department (ED) with a suspected ACS are enrolled and randomized within 6 weeks of their ED visit. The primary outcome, FoR, is measured by the adapted Concerns about Recurrent ACS Scale. The trial also tests the intervention's effect on a potential mechanism of health behavior change that is inversely correlated with fear: an expansive future time perspective. Additional outcomes include electronically measured adherence to a cardiovascular medication and self-reported physical activity. Conclusions: This study takes a mechanistic approach to addressing the dangerous problem of poor health behaviors after ACS. The trial will test whether targeting FoR or future time perspective by CBMT is a promising approach to improving nonadherence after ACS.

Changes in the intestinal lymphatic vascular system, such as lymphatic obstruction, are characteristic features of inflammatory bowel diseases. The lymphatic vasculature forms a conduit to enable resolution of inflammation; this process is driven by specialized endogenous proresolving mediators (SPMs). To evaluate contributions of lymphatic obstruction to intestinal inflammation and to study profiles of SPMs, we generated a novel animal model of lymphatic obstruction using African green monkeys. Follow-up studies were performed at 7, 21, and 61 days. Inflammation was determined by histology. Luminex assays were performed to evaluate chemokine and cytokine levels. In addition, lipid mediator metabololipidomic profiling was performed to identify SPMs. After 7 days, lymphatic obstruction resulted in a localized inflammatory state, paralleled by an increase in inflammatory chemokines and cytokines, which were found to be up-regulated after 7 days but returned to baseline after 21 and 61 days. At the same time, a distinct pattern of SPMs was profiled, with an increase for D-series resolvins, protectins, maresins, and lipoxins at 61 days. These results indicate that intestinal lymphatic obstruction can lead to an acute inflammatory state, accompanied by an increase in proinflammatory mediators, followed by a phase of resolution, paralleled by an increase and decrease of respective SPMs.

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