Tofacitinib, a JAK inhibitor targeting predominantly JAK1 and JAK3, has been approved for the treatment of ulcerative colitis (UC), and there are other specific JAK inhibitors under development that may be effective in Crohn's.
In summary, our study outlines the contribution of non-coding variants in neutrophil GM-CSF signaling and the potential importance of RCL1 and AK3 in CD pathogenesis.
Crohn's disease (CD), ulcerative colitis (UC) and inflammatory bowel disease (IBD) associated with primary sclerosing cholangitis (PSC-IBD), share three major pathogenetic mechanisms of inflammatory bowel disease (IBD)-gut dysbiosis, gut barrier failure and immune system dysregulation.
Furthermore, IncRNA ANRIL expression was increased after infliximab treatment compared with baseline in patients with A-CD that responded to treatment (P < 0.001) but remained stable in patients with A-CD that did not respond (P = 0.897).
Our findings suggest that HPM in treating Crohn's disease functions possibly via upregulation of the A20 expression level, resulting in downregulation of TNFR1, TRADD, and RIP1 to alleviate increased cell apoptosis in the intestinal epithelial barrier in Crohn's disease.
The aims of this pilot study performed in patients with CD after ileocolonic resection were to compare the macroscopic appearance of the neoterminal ileum, according to the endoscopic Rutgeerts score, with the microscopic findings provided by CLE 6 to 12 months after surgery and to assess the predictive values of CLE-generated parameters for predicting further recurrence in patients with postoperative endoscopic remission.
AIEC bacteria survival increased in patients with CD-associated polymorphism <i>IRGM</i> (<i>p</i> = 0.05) and reduced in those with CD-associated polymorphisms <i>XBP-1</i> (<i>p</i> = 0.026) and <i>ULK-1</i> (<i>p</i> = 0.033).
To investigate effects moxibustion exerts on A20 expression and regulation of intestinal epithelial tight junctions via the TNF-α-NF-κB-MLCK pathway in Crohn's disease (CD).
We examined transcriptional data from CD mucosa for evidence of CSF-1 pathway activation and tested JNJ-40346527 (PRV-6527), a small molecule inhibitor of CSF-1 receptor kinase (CSF-1R), for its ability to inhibit disease indices in murine colitis.
Our results suggest that oxidative stress-induced DNA methylation of miR-122 aggravates colitis targeting SELENBP1 partially by p65NF-<i>κ</i>B signaling and may promote the progression of CD.
To investigate effects moxibustion exerts on A20 expression and regulation of intestinal epithelial tight junctions via the TNF-α-NF-κB-MLCK pathway in Crohn's disease (CD).
We report the 11 cases of +8-MDS/MPN associated with Behcet's-like syndrome and compare them with Behcet's disease and Crohn's disease, pool with literature cases for analysis.
Of note, the hub genes G protein subunit gamma 11 (GNG11), G protein subunit beta 4 (GNB4), Angiotensinogen (AGT), Phosphoinositide-3-kinase regulatory subunit 3 (PIK3R3) and C-C motif chemokine receptor 7 (CCR7) are disease-specific and may be used as biomarkers for differentiating UC from CD.
MCs, VIP, and VIP-receptors (VPACs) were quantified by immunofluorescence and enzyme-immunoassay (EIA) in ileal tissues (villus epithelium (VE) and adjacent VE, ie, VE next to the follicle-associated epithelium, (FAE)) from Crohn's disease (CD; n = 16) and non-IBD patients, and in colonic specimens of ulcerative colitis (UC; n = 12) and healthy controls (HCs).
Our results suggest the use of miR-27a/191 for Crohn's disease small bowel, none of the five candidate genes for Crohn's disease colon, and miR-16/27a for ulcerative colitis.
The difference is most evident for the rate of Met-enkephalin degradation between men (mean T<sub>1/2</sub> = 13.61 min) and women (mean T<sub>1/2</sub> = 21.84 min) with Crohn's disease (CD).
Intestinal biopsies of 30 patients (12 male and 18 female; mean age, 34 years; range 4-77 years) with the confirmed diagnosis of Crohn's disease and 30 patients diagnosed as non-inflammatory bowel disease (19 male and 11 female; mean age, 38 years; range 13-68 years) were studied by molecular, histopathological and histochemical methods.