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Increased expression of interleukin 17 in inflammatory bowel disease
TLDR
It is likely that IL-17 expression in IBD may be associated with altered immune and inflammatory responses in the intestinal mucosa and increased in patients with inflammatory bowel disease.
Interleukin-22, a member of the IL-10 subfamily, induces inflammatory responses in colonic subepithelial myofibroblasts.
TLDR
IL-22 derived from activated T cells acts on SEMFs to elicit expression of proinflammatory cytokines and matrix-degrading molecules indicating proinflammatory/remodeling roles in IBD.
Interleukin-33 expression is specifically enhanced in inflamed mucosa of ulcerative colitis
TLDR
IL-33, derived from colonic SEMFs, may play an important role in the pathophysiology of UC, and is characterized by real-time polymerase chain reaction (PCR) and immunohistochemical methods.
Cross-sectional imaging in Crohn disease.
TLDR
CT or MR imaging should be included in a comprehensive evaluation of patients with Crohn disease, along with conventional imaging and clinical and laboratory tests, thereby aiding in treatment planning.
Comparison of the fecal microbiota profiles between ulcerative colitis and Crohn’s disease using terminal restriction fragment length polymorphism analysis
TLDR
The gut microbiota of patients with inactive UC tended to be closer to that of healthy individuals, suggesting different roles for the fecal microbiota in the pathophysiology of UC and CD.
Multicenter analysis of fecal microbiota profiles in Japanese patients with Crohn’s disease
TLDR
Dysbiosis in CD patients was shown by a multi-IBD center study and a logistic model to predict disease activity based on the fecal microbiota composition was developed, which proposed the feasibility of using the feces profile as a predictive marker for disease activity.
Terminal restriction fragment length polymorphism analysis of the diversity of fecal microbiota in patients with ulcerative colitis
TLDR
The diversity of fecal microbiota in patients with UC was different from that in healthy individuals, and the T‐RFLP patterns were different between the active patients and inactive (remission) patients.
Expression of IL-24, an Activator of the JAK1/STAT3/SOCS3 Cascade, Is Enhanced in Inflammatory Bowel Disease
TLDR
IL-24 derived from colonic SEMFs acts on colonic epithelial cells to elicit JAK1/STAT-3 activation and the expression of SOCS3 and mucins, supporting their suppressive effects on mucosal inflammation in IBD.
Epithelial overexpression of interleukin-32alpha in inflammatory bowel disease.
TLDR
Epithelial IL-32alpha expression was increased in IBD patients, and in CD patients in particular, and might be involved in the pathophysiology of IBD as a proinflammatory cytokine and a mediator of innate immune response.
The multidrug-resistance protein 4 polymorphism is a new factor accounting for thiopurine sensitivity in Japanese patients with inflammatory bowel disease
TLDR
The results suggest that MRP4 G2269A might be a new factor accounting for thiopurine sensitivity in Japanese patients with IBD.
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