Wound infection prevention strategies in colorectal endoscopic mucosal resection: A meta-analysis of prophylactic measures.

Colorectal endoscopic mucosal resection (EMR) is associated with the risk of postoperative wound infections, prompting investigations into effective prophylactic measures. This meta-analysis aimed to evaluate the efficacy of various prophylactic interventions in reducing the incidence of wound infections following EMR. Adhering to PRISMA guidelines, we conducted a comprehensive search across multiple databases for randomized controlled trials (RCTs) and cohort studies from 2015 to 2022. We included studies that compared the efficacy of antibiotic prophylaxis and antiseptic measures, with clear data on post-procedure infection rates. Eight studies met our inclusion criteria, and data were extracted for meta-analysis. The risk of bias was assessed using the Cochrane Collaboration tool and the Newcastle-Ottawa Scale. The meta-analysis included 3765 patients from eight RCTs. Prophylactic antibiotics (cefixime and cefuroxime) showed moderate to high efficacy, with infection rates as low as 0% and 0.76%. Prophylactic endoscopic closure and clipping showed the highest efficacy, with zero reported infections. The standardized surgical site infection prevention bundle had lower effectiveness, with an infection incidence of 3.83%. The risk of bias assessment indicated potential performance bias due to lack of blinding, but overall evidence quality was upheld by proper random sequence generation and diligent outcome data monitoring. The effectiveness of specific prophylactic measures, notably prophylactic antibiotics and mechanical closure techniques, has been shown in significantly reducing the risk of wound infections following colorectal EMR.

IL-9 antibody injection suppresses the inflammation in colitis mice.

Diverse T help (Th) cells play a crucial role in the processing and maintaining of chronic inflammation as seen in ulcerative colitis (UC). Th9, a novel subset of Th cells that primarily produces interleukin (IL)-9, has recently been associated with the development of inflammatory diseases. In this study, we evaluated the presentation of Th9 cells in inflamed tissues of human and experimental mouse UC, and examined the therapeutic efficiency of anti Th9 cytokine IL-9 in the experimental mouse UC. Using immunohistochemistry (IHC), we evaluated the presentation of Th9 cells labelled by transcriptional factor PU.1 in both human and dextran sulfate sodium (DSS) induced mouse colitis biopsies. The results showed that increased PU.1 positive Th9 cells were mainly located in the lamina propria in relative with the controls, intraepithelial Th9 cells can also be observed but at low density. Double IHCs revealed that most of PU.1 positive cells were CD3 positive lymphocytes in human UC specimens. Anti-IL-9 antibody injection for 2 weeks reduced the severity of inflammation in DSS induced colitis mice. Our results suggest that The Th9/IL-9 is involved in the pathogenesis of UC.

Therapeutic efficacy of IL-17A antibody injection in preventing the development of colitis associated carcinogenesis in mice.

Chronic inflammation increases colorectal cancer (CRC) risk as seen in ulcerative colitis (UC). Proinflammatory cytokines play a critical role in mediating the development of colitis associated cancer (CAC). In this study, the therapeutic efficacy of anti-interleukin (IL)-17A by anti-IL-17A antibody injection on the development of CAC was assessed in 1,2-dimethylhydrazine (DMH) plus dextran sulfate sodium (DSS) induced CAC mouse model. The results showed that mice dosed with DMH plus DSS for 10 weeks evoked high degree dysplastic lesion in the large bowel that accompanied with significant increased IL-17A expression, proliferation index and inflammation degree in mice. After anti-IL-17A antibody injection for 2 weeks, the number of tumors, proliferation index and the expression level of IL-17A protein in the large bowel tissues were significantly decreased. Therefore, we concluded that the anti-IL-17A blockade can suppress the development of CAC and is a potential therapeutic agent for the prevention of CAC in colitis mice.

Dynamics of the IL-33/ST2 network in the progression of human colorectal adenoma to sporadic colorectal cancer.

Most sporadic colorectal cancers (CRCs) develop from preformed adenomas. Cytokines are involved in the transition from adenoma to CRC. Interleukin-33 (IL-33) is a newly discovered proinflammatory cytokine belonging to the IL-1 cytokine family and involved in the development of chronic inflammation and cancer. The aim of this study was to evaluate the dynamics of the IL-33/ST2 axis during the sequence of progression from normal colorectum to adenoma to carcinoma and to investigate the association of IL-33 and ST2 expression with clinicopathological parameters and prognosis. The results demonstrated that the levels of IL-33 and ST2 in adenomas (n = 50), determined by real-time PCR, were significantly higher than those of normal controls (n = 30); the levels of both IL-33/ST mRNA in CRCs (n = 50) were higher than in normal controls but lower than in adenomas. Further analysis revealed that the expression level of ST2 in CRCs was associated with tumor/node/metastasis (TNM) stage. The log-rank test showed that neither the IL-33 nor the ST2 expression level was correlated with overall survival in patients with CRC. The increased expression of IL-33/ST2 in adenomas and CRC tissues was confirmed by immunohistochemistry and was observed in both the tumor stromal cells and adenomatous/cancerous cells. Notably, increased densities of IL-33-positive and ST2-positive microvessels were found in the stroma of adenomas and CRCs. In conclusion, increased expression of the IL-33/ST2 axis along the colorectal adenoma-carcinoma sequence might be involved in the neoplastic transformation via the participation of this axis in the regulation of angiogenesis.

Involvement of NF-κB/IL-6 Pathway in the Processing of Colorectal Carcinogenesis in Colitis Mice.

Nuclear factor-kappaB (NF-κB)/interleukin (IL-6) pathway links chronic inflammation to colitis associated cancer (CAC). In this study, we examined the dynamic temporal changes of the NF-κB/IL-6 pathway during the procession of experimental CAC mouse model. Mice were sacrificed after induction for 14, 16, 18, and 22 weeks for the examination of tumor burden, inflammation degree, and protein level of NF-κB and IL-6 in bowel tissues. The results showed that tumor burden and inflammation severity in the bowels were gradually increased over the observed time-points. The expressions of IL-6 and NF-κB proteins were gradually increased after induction of dysplastic lesions over times. These data provide new information on the dynamic temporal changes of NF-κB/IL-6 pathway in relation to CAC development that may be relevant in the design of future investigations of therapeutic interventions to effectively target CAC processes.

The role of interleukin-17A in colorectal tumorigenesis.

It has been well documented that interleukin (IL)-17A mainly produced by the newly identified T cell subtype Th17 cells is an important proinflammatory cytokine that plays a vital pathogenic role in the process of human inflammatory bowel diseases. Recently, new information concerning the biological activities of IL-17A relating to the development of colorectal cancer (CRC) has also been reported. The present mini-review focuses on recent observations concerning the role of IL-17A in the development of CRCs, and it discusses the clinical significance of IL-17A as a biomarker and potential therapeutic target.