05), increased abundance of Bacteroidetes (P = 0.014) and Synegitestes (P = 0.017), and reduced abundance of Actinobacteria (P = 0.004). The classes Flavobacteria (P = 0.028) and Epsilonproteobacteria (P = 0.017) were less enriched in IBS. Abundance differences were largely consistent from the phylum to genus level. Probiotic treatment in IBS patients was associated with a significant reduction of the genus Bacteroides (all taxonomy levels; P < 0.05) to levels similar to that of controls.

Epacadostat supplier In this pilot study, global and deep molecular analysis demonstrates an altered mucosal microbiota composition in IBS. Probiotic leads to detectable changes in the microbiota. These effects of probiotic bacteria may contribute to their therapeutic benefit. “
“See article in J. Gastroenterol. Hepatol. 2011; 26: 1298–1308. Inflammatory bowel disease (IBD), which includes Crohn’s disease and ulcerative colitis (UC), is a chronic and relapsing inflammatory disorder in the gut. Although new therapeutic

agents, such as biological agents, have been developed, Pexidartinib current medical treatments do not provide a non-relapsing cure. Patients with long-standing IBD are at increased risk of developing colitis-associated colon cancer (CAC), which is a life-threatening complication.1 Thus, more effective and safer therapeutic agents for the treatment of IBD and the prevention of CAC are needed. Although there have been significant advances in the identification of susceptible genes through genome-wide association studies, the etiopathogenesis of IBD remains unclear. However, it is generally accepted that IBD is attributable to the interaction between genetic, microbial, and host immunological factors. Recently, convincing evidence has been adduced that gut microbiota play a pivotal role in the pathogenesis of intestinal inflammation. Interleukin-2 receptor Animal models of colitis under germ-free conditions remain healthy, whereas they subsequently develop intestinal inflammation after transferring to non-sterile environments or colonization with commensal flora.2,3 In addition,

several studies have shown a remarkable shift in microbial profiles among patients with IBD.4–6 Further, some bacteria can reduce intestinal permeability, thereby preventing exposure of the immune system to luminal antigens, such as food or pathogenic bacteria.7 A recent study using germ-free and gnotobiotic technology demonstrated that gut microbiota were necessary for the development of CAC, while the severity of chronic colitis was correlated with colorectal tumor development.8 In addition, gut microbiota have homeostatic immune and metabolic functions, and modulate epithelial cell survival and proliferation.9 These findings suggest that gut microbiota play an important role in CAC in a susceptible host. Meanwhile, Bifidobacterium lactis ameliorated murine colitis and colitic cancer by the inhibition of nuclear factor-κB signaling.