Class A1 scavenger receptor antibody improves murine colitis by influencing macrophage and gut microbiota.

This study aimed to investigate whether class A1 scavenger receptor (SR-A1) regulated macrophage polarization and gut microbial alteration during intestinal inflammation of colitis. A murine colitis model was established by feeding with dextran sulfate sodium (DSS), and treatment groups were injected intravenously with SR-A1 antibody. Results showed a preventive effect on colitis symptoms and fewer inflammatory cell infiltrates in treatment groups.

Capsulized Fecal Microbiota Transplantation Induces Remission in Patients with Ulcerative Colitis by Gut Microbial Colonization and Metabolite Regulation.

Fecal microbiota transplantation (FMT) can induce clinical remission in ulcerative colitis (UC) patients. Enemas, nasoduodenal tubes, and colonoscopies are the most common routes for FMT administration. However, there is a lack of definitive evidence regarding the effectiveness of capsulized FMT treatment in UC patients.

Specific fungi associated with response to capsulized fecal microbiota transplantation in patients with active ulcerative colitis.

Objective: Fecal microbiota transplantation (FMT) is a novel microbial treatment for patients with ulcerative colitis (UC). In this study, we performed a clinical trial of capsulized FMT in UC patients to determine the association between the gut fungal community and capsulized FMT outcomes.

Design: This study recruited patients with active UC (N = 22) and healthy individuals (donor, N = 9) according to the criteria.

Decreased serum iron concentration and total iron binding capacity are associated with serious Crohn's disease.

This study aimed to investigate whether serum indicators related to iron stores in the body are associated with clinical and endoscopic disease severity. Eighty-four patients with Crohn's disease (CD) and twenty-four healthy volunteers were included. The indicators related to iron stores were detected within one week after endoscopic and CT enterography examinations.

The Development and Validation of Anti-paratuberculosis-nocardia Polypeptide Antibody [Anti-pTNP] for the Diagnosis of Crohn's Disease.

Background And Aims: Non-invasive biomarkers in sera of patients with inflammatory bowel disease [IBD] are not currently available for rapidly and accurately diagnosing the disease. We aimed to investigate and validate the potential roles of anti-paratuberculosis-nocardia polypeptide antibodies [anti-pTNP] in the diagnosis of IBD.

Methods: Serum samples were collected from 502 patients with diagnosed Crohn's disease [CD], 141 patients with ulcerative colitis [UC], and 109 healthy donors.

Class A1 scavenger receptors mediated macrophages in impaired intestinal barrier of inflammatory bowel disease.

Background: This study was to investigate the cytokines and phenotype of macrophages pre-treated with class A1 scavenger receptor (SR-A1) antibody in vitro and the influence on apoptotic pathway of colonic epithelial cells, and to explore the role of SR-A1 mediated macrophages in impaired intestinal barrier of inflammatory bowel diseases (IBDs).

Methods: Mouse macrophage RAW264.7 was pre-treated with SR-A1 antibody in the presence of lipopolysaccharide (LPS).

Elevated serum triglyceride and low-density lipoprotein cholesterol promotes the formation of colorectal polyps.

Background: Hyperlipidaemia may be a potential risk factor for the occurrence of intestinal polyps. This study aimed to evaluate correlation between lipidaemia and the formation of colorectal polyps.

Methods: One hundred and fourteen patients with colorectal polyps and forty-eight healthy controls were included in this study.

Synergistic effect of enteral nutrition on remission induction in a patient with penetrating Crohn disease: A case report.

Rationale: Crohn disease includes 3 phenotypes, inflammatory, stricturing, and penetrating. In cases where corticosteroids and immunosuppressive agents are not suitable treatment options, enteral nutrition (EN) can be used to reduce disease severity and enhance barrier defense with fewer potential adverse effects.

Patient Concerns: A 23-year-old man with abdominal pain and diarrhea presented at our hospital in 2014.

Interleukin-25 enhances the capacity of mesenchymal stem cells to induce intestinal epithelial cell regeneration.

Background: This study aimed to investigate the influence of IL-25 on the capacity of mesenchymal stem cells (MSCs) to induce intestinal epithelial cell regeneration.

Methods: The CD4IL-25R cells and LGR5IL-25R cells in colonic mucosa of Crohn's disease (CD) patients, ulcerative colitis (UC) patients and healthy controls were detected by immunofluorescence staining, and the CD4IL-25R cells in peripheral blood were detected by flow cytometry. Rat MSCs were separated and stimulated with IL-25.

Interleukin-25 primed mesenchymal stem cells achieve better therapeutic effects on dextran sulfate sodium-induced colitis via inhibiting Th17 immune response and inducing T regulatory cell phenotype.

Aim: This study aimed to investigate the anti-inflammatory mechanism of IL-25 mediated mesenchymal stem cells (MSC) treatment for inflammatory bowel disease (IBD) in a DSS-induced rat colitis model.

Methods: Rats with DSS-induced colitis were divided into control and treatment groups: normal control group (rats fed with water), DSS group (rats fed with DSS solution), MSC group (DSS-treated rats injected intravenously with GFP-MSCs), IL-25-MSC group (DSS-treated rats injected intravenously with IL-25 primed GFP-MSCs), and mesalazine group (DSS-treated rats fed with mesalazine).

Results: In IL-25-MSC group, therapeutic efficacy (clinical symptoms) was better than in MSC group, but comparable to mesalazine group.

IL-25 downregulates Th1/Th17 immune response in an IL-10-dependent manner in inflammatory bowel disease.

Background: Interleukin 25 (IL-25) is involved in the initiation of T helper cell (Th)2-mediated immunopathologies. In this study, we investigated the expression of IL-25 in inflammatory bowel disease (IBD) and its role in the induction of CD4 T-cell differentiation.

Methods: Expression of IL-25 in inflamed mucosa of patients with IBD was determined by quantitative real-time polymerase chain reaction, immunohistochemistry, and enzyme-linked immunosorbent assay.

Interleukin (IL)-23 suppresses IL-10 in inflammatory bowel disease.

Interleukin (IL)-10 plays an important role in immune regulation in the intestine. Immune deregulation is suggested in the pathogenesis of inflammatory bowel disease (IBD). This study aims to elucidate the role of IL-23 in the suppression of IL-10 in the IBD intestinal mucosa.

The increased expression of IL-23 in inflammatory bowel disease promotes intraepithelial and lamina propria lymphocyte inflammatory responses and cytotoxicity.

This study analyzed IL-23p19 expression in inflamed mucosa of IBD and the role in the induction of IEL and NK cell activation as well as Th17 cell differentiation. Expression of IL-23p19 was performed by immunohistochemistry and quantitative real-time PCR. Expression of IL-23R was assessed by flow cytometry.