Globally, colorectal cancer (CRC) is one of the leading causes of health problems. More reliable molecular biomarkers for early diagnosis in CRC patients are needed. A crucial role for thyroid hormone receptor interacting protein 6 (TRIP6) is played in tumorigenesis and tumor growth. Our study aims to determine the diagnostic and prognostic roles of TRIP6 at CRC. TRIP6 gene expression levels were analyzed in this study from public databases. The relationship between TRIP6 expression and clinicopathological characteristics was explored by logistic regression analysis. Based on Kaplan–Meier (K–M) survival curves and receiver operating characteristic curves (ROC) analysis, the prognostic and diagnostic values of TRIP6 were determined. Protein–protein interaction (PPI) networks analysis were performed using the STRING database. A Spearman's correlation analysis applied for examining the correlation between TRIP6 expression, immune cell infiltration, and immune checkpoint genes. Moreover, colony formation assay and transwell assay were used to investigate the functions of TRIP6. TRIP6 was highly expressed in CRC cancer tissues and cells. K-M survival analysis indicated that a high expression of TRIP6 was associated with poor prognosis. TRIP6 expression was obviously associated with immune cell infiltration and immune checkpoint gene expression. For validation, the results of collected clinical CRC samples show that TRIP6 levels in CRC tumor tissue were higher than those of paired adjacent colorectal tissues. Additionally, in vitro experiments suggested that TRIP6 knockdown suppressed proliferation and migration in CRC cell line RKO. TRIP6 overexpression promoted the proliferation and migration of normal colon cell line NCM460. High TRIP6 expression is associated with poor prognosis in colorectal cancer and promotes tumor cell proliferation and migration which may be a potential diagnostic and prognostic biomarker and a promising therapeutic target for CRC, providing new insights into its role in CRC.

GSDMB-mediated pyroptosis facilitates a pro-inflammatory immune microenvironment and needs to be tightly regulated to avoid excessive inflammation. Here, we provide evidence that itaconate and its cell-permeable derivative 4-octyl itaconate (4-OI) can significantly inhibit GSDMB-rendered pyroptotic activity independent of Nrf2. 4-OI interferes proteolytic process of GSDMB by directly modifying Cys54, Cys148 and Ser212 on granzyme A (GrzA), a serine protease that site-specifically cleaves the inter-domain linker of GSDMB, instead of interaction with GSDMB, thereby blocking pyroptosis and exerts anti-inflammatory effects. Moreover, 4-OI alleviates inflammation by suppressing GSDMB-induced pyroptotic cell death during acute colitis models in intestinal epithelial GSDMB conditional transgenic mice. Our data expand the role of 4-OI as a crucial immunometabolic derivative that regulates innate immunity and inflammation through a newly identified posttranslational modification, and targeting of pyroptosis by 4-OI therefore holds potent therapeutic potential for primarily inflammatory and/or autoimmune diseases.

Gasdermins (GSDMs) protein family express in intestinal epithelial cells or lamina propria immune cells, and play a nonnegligible function during gut homeostasis. With the gradually in-depth investigation of GSDMs protein family, the proteases that cleave GSDMA-E have been identified. Intestinal GSDMs-induced pyroptosis is demonstrated to play a crucial role in the removal of self-danger molecules and clearance of pathogenic organism infection by mediating inflammatory reaction and collapsing the protective niche for pathogens. Simultaneously, excessive pyroptosis leading to the release of cellular contents including inflammatory mediators into the extracellular environment, enhancing the mucosal immune response. GSDMs-driver pyroptosis also participates in a novel inflammatory cell death, PANoptosis, which makes a significant sense to the initiation and progression of gut diseases. Moreover, GSDMs are expressed in healthy intestinal tissue without obvious pyroptosis and inflammation, indicating the potential intrinsic physiological functions of GSDMs that independent of pyroptotic cell death during maintenance of intestinal homeostasis. This review provides an overview of the latest advances in the physiological and pathological properties of GSDMs, including its mediated pyroptosis, related PANoptosis, and inherent functions independent of pyroptosis, with a focus on their roles involved in intestinal inflammation and tumorigenesis.

The pH value in the wound milieu plays a key role in cellular processes and cell cycle processes involved in the process of wound healing. Here, a microfluidic assembly technique is employed to fabricate micro-gel ensembles that can precisely tune the pH value of wound surface and accelerate wound healing. The micro-gel ensembles consist of poly (hydroxypropyl acrylate-co-acrylic acid)-magnesium ions (poly-(HPA-co-AA)-Mg2+ ) gel and carboxymethyl chitosan (CMCS) gel, which can release and absorb hydrogen ion (H+ ) separately at different stages of healing in response to the evolution of wound microenvironment. By regulating the wound pH to affect the proliferation and migration of cell on the wound and the activity of various biological factors in the wound, the physiological processes are greatly facilitated which results in much accelerated healing of chronic wound. This work presents an effective strategy in designing wound healing materials with vast potentials for chronic wound management.

Background With the increasing demand for individualized treatment in Crohn’s disease, a score for accurate evaluation of inflammation grade will be of great significance. We have developed the JINLING score to assess inflammation severity for Crohn’s disease, which incorporates an endoscopic score (SES-CD) and a 2-item patient-reported outcome (PRO2). The aim of this study was to examine the performance of JINLING score in evaluating inflammation grade and the correlation with the clinical outcomes. Methods The correlation between JINLING score and Global Histologic Disease Activity Score (GHAS), fecal calprotectin (FCP), and C-reactive protein (CRP) level was performed in an exploration phase with a retrospective data set. The data on clinical outcomes including medication effects, Crohn’s disease-related surgery and biochemical results were collected from a single-center prospective validation cohort. Results JINLING score correlated significantly with FCP, CRP, and hemoglobin in the exploration cohort (all P < 0.05). The receiver operating characteristic (ROC) curves based on a threshold Crohn’s disease activity index value of 150, GHAS of 4, and FCP of 60 μg/g to identify disease activity, all showed a higher area under the curve with JINLING score than SES-CD or PRO2 alone. In the validation cohort, patients with high inflammation grade (JINLING ≥4) had higher GHAS, CRP, and FCP than low inflammation grade patients. High JINLING score was associated with an increased risk of treatment failure (hazard ratio 2.93; 95% confidence interval 1.13–7.61, P = 0.021). Conclusion This newly developed index served well for quantifying inflammation grade and predicting clinical outcomes. JINLING score has the potential to facilitate clinical decision-making and personalized therapy for Crohn’s disease patients.

BACKGROUND:Macrophage-inducible C-type lectin [Mincle] signalling plays a proinflammatory role in different organs such as the brain and liver, but its role in intestinal inflammation, including Crohn's disease [CD], remains unknown.METHODS:The characteristics of Mincle signalling expression in CD patients and experimental colitis were examined. The functional role of Mincle signalling in the intestine was addressed in experimental colitis models in vivo by using Mincle knock-out [Mincle-/-] mice. In addition, neutralising anti-Mincle antibody, downstream spleen tyrosine kinase [Syk] inhibitor, and Mincle pharmacological agonist were used to study the Mincle signalling in intestine. Bone marrow-derived macrophages were collected from mice and used to further verify the effect of Mincle signalling in macrophages.RESULTS:This study has shown that Mincle signalling was significantly elevated in active human CD and experimental colitis, and macrophages were the principal leukocyte subset that upregulate Mincle signalling. Mincle deficiency and Syk pharmacological inhibition ameliorated the colitis by reducing induced macrophage pyroptosis, and activation of Mincle with the agonist aggravated the intestinal inflammation. The ex vivo studies demonstrated that activation of Mincle signalling promoted the release of proinflammatory cytokines, whereas its absence restricted release of proinflammatory cytokines from pyroptosis of macrophages. In addition, Mincle/Syk signalling in macrophages could promote the production of chemokines to recruit neutrophils by activating mitogen-activated protein kinase [MAPK] during intestinal inflammation.CONCLUSIONS:Mincle signalling promotes intestinal mucosal inflammation by inducing macrophage pyroptosis. Modulation of the Mincle/Syk axis emerges as a potential therapeutic strategy to target inflammation and treat CD.

The role of spliceosome-associated protein 130 (SAP130) in gut inflammation, particularly in Crohn's disease (CD), remains unclear. The aim of our study was to analyze correlations between serum SAP130 levels and CD severity, and to assess its predictive value for the clinical efficacy of exclusive enteral nutrition (EEN) in CD. Correlations between the SAP130 levels and CD severity were evaluated. SAP130 and its receptor Mincle (macrophage-inducible C-type lectin) in the colon tissue in active CD were measured. Furthermore, the serum SAP130 level was investigated as a predictor of clinical efficacy in patients treated with EEN. The serum SAP130 levels significantly increased in patients with active CD compared with patients in remission for CD (P < 0.001) and control individuals (P < 0.001), and they varied according to clinical activity and significantly correlated with disease severity. In parallel, the expression of both SAP130 and Mincle in colon tissue was elevated in active CD. Additionally, the serum SAP130 level declined in patients with active CD who achieved efficacy at week 8 after EEN therapy. This preliminary evidence shows that SAP130 might be a potential noninvasive biomarker that correlates well with CD severity and the clinical efficacy of EEN in CD.

Long non-coding RNAs (lncRNAs) are essential contributors to the progression of various human cancers. Long intergenic non-protein coding RNA 1106 is a member of lncRNAs family. Until now, the specific role of LINC01106 in CRC remains undefined. The aim the current study was to unveil the functions of LINC01106 and explore its potential molecular mechanism in CRC. Based on the data of online database GEPIA, we determined that LINC01106 was expressed at a high level in colon adenocarcinoma (COAD) tissues compared to normal colon tissues. More importantly, high level of LINC01106 had negative correlation with the overall survival of COAD patients. Additionally, we also determined the low level of LINC01106 in normal colon tissues based on UCSC database. Through qRT-PCR, we identified that LINC01106 was highly expressed in CRC tissues compared to adjacent normal ones. Similarly, we detected the expression of LINC01106 and confirmed that LINC01106 was expressed higher in CRC cells than that in normal cells. Subsequently, LINC01106 was mainly distributed in the cytoplasm. LINC01106 induced the proliferation, migration, and stem-like phenotype of CRC cells. Mechanistically, cytoplasmic LINC01106 positively modulated Gli4 in CRC cells by serving as a miR-449b-5p sponge. Furthermore, nuclear LINC01106 could activate the transcription of Gli1 and Gli2 through recruiting FUS to Gli1 and Gli2 promoters. Mechanism of investigation unveiled that Gli2 was a transcription activator of LINC01106. In conclusion, Gli2-induced upregulation of LINC01106 aggravates CRC progression through upregulating Gli2, Gli2, and Gli4.

Background: It is of crucial importance to evaluate disease activity by means of endoscopy and histopathology in Crohn's disease (CD). Nonetheless, correlation between endoscopic and histological validated indices has not been verified. Aims: We aim to correlate the Simple Endoscopic Score for Crohns disease (SES-CD) with two validated widely used histological indices in patients with established CD. Methods: The SES-CD at the worst affected area was scored and histological disease activity using Global Histologic Disease Activity Score (GHAS or D'Haens score) and the Naini and Cortina Score (NCS) was scored independently by two pathologists blinded to the clinical information and endoscopic results. Spearman correlation between the SES-CD, GHAS and NCS were performed. Results: 143 patients, 32 with SES-CD scores 0-2, 57 with 3-6, 37 with 7-15, and 17 with >= 16. Correlation coefficients between SES-CD and GHAS were r = 0.86 (95% CI 0.80-0.91, p < 0.001) and between SES-CD and NCS r = 0.85 (95% CI 0.81-0.88, p < 0.001). There was a strong correlation between the two histological indices (r = 0.70, 95% CI 0.59-0.78, p < 0.001). Mucosal healing without histological disease activity was most correlated with SES-CD score 0 or 1. Conclusions: The SES-CD strongly correlates with both GHAS and NCS. The SES-CD of 0 to 1 best represents histological remission that correlates with quiescent disease activity. (C) 2019 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.

BackgroundNecrotizing soft tissue infections (NSTIs) is severe surgical infections which can occur following trauma or abdominal surgery. NSTIs secondary to gastrointestinal (GI) fistula is a rare but severe complication.MethodsA retrospective cohort study was performed on all subjects presenting with GI fistulas associated NSTIs were included. Clinical characteristics, microbiological profile, operations performed, and outcomes of patients were analyzed.ResultsBetween 2014 and 2017, 39 patients were finally enrolled. The mean age were 46.9years and male were the dominant. For the etiology of fistula, 25 (64.1%) of the patients was due to trauma. Overall, in-hospital death occurred in 15 (38.5%) patients. Microbiologic findings were obtained from 31 patients and Klebsiella pneumoniae was the most common species (41.0%). Eight patients were treated with an open abdomen; negative pressure wound therapy was used in 33 patients and only 2 patients received hyperbaric oxygen therapy. Younger age and delayed abdominal wall reconstruction repair were more common in trauma than in non-trauma. Non-survivors had higher APACHE II score, less source control<48h and lower platelet count on admission than survivors. Multiple organ dysfunction syndrome, multidrug-resistant organisms and source control failure were the main cause of in-hospital mortality.ConclusionsTrauma is the main cause of GI fistulas associated NSTIs. Sepsis continues to be the most important factor related to mortality. Our data may assist providing enlightenment for quality improvement in these special populations.

Background: From prior works, aggressive tumor cell growth, stemness, migration, and invasion are related to oncogenesis. Long non-coding RNA LINC01106 is overexpressed and decreases overall survival time of COAD (Colon adenocarcinoma) patients, as annotated in bioinformatics website GEPIA. Therefore, the study is to define the unclear biological function of LINC01106 in CRC (colorectal cancer). Methods: qRT-PCR, FISH and subcellular fractionation probed LINC01106 expression and distribution in CRC cells. CRC cell growth was determined in the absence of LINC01106 via EdU and colony formation. The effects of LINC01106 on CRC migration, invasion and EMT were monitored using transwell assay and western blot. Stemness of CRC cells was examined via sphere formation. LINC01106-mediated mechanism was monitored via ChIP, luciferase reporter, RNA pull-down followed by silver staining, and RIP assays. Results: Our data supported that LINC01106 induced malignant proliferation and stem-like phenotypes in CRC cells. Mechanistically, cytoplasmic LINC01106 sponged and suppressed miR-449b-5p in CRC cells. Moreover, online data showed that LINC01106 was positively correlated with Gli4 level in COAD tissues. Gli4 elevation predicted dreadful survival of COAD patients. Mechanical assays confirmed that LINC01106 could increase Gli4 expression as a miR-449b-5p sponge. Furthermore, nuclear LINC01106 interacted with FUS to Gli1 and Gli2 promoters for Gli1 and Gli2 transcriptional elevation, resulting in Hedgehog signaling transduction. Intriguingly, Gli2 was a transcription initiator of LINC01106. Rescue experiments elaborated that Gli1, Gli2, Gli4, and Hedgehog pathway agonist SAG could antagonize LINC01106-modulated CRC growth aggressiveness, and stemness. Rescue experiments confirmed LINC01106-mediated intermolecular functions in CRC growth and stemness. Conclusion: Previously unrecognized LINC01106 was functionally and mechanically characterized in CRC. It introduced that Gli2-induced LINC01106 could aggravate CRC progression through post-transcriptional or transcriptional promotion of Gli family proteins. It is expected to impart innovative avenues for generating CRC therapeutic approaches. Funding Statement: This work was supported by Jiangsu Provincial Natural Science Fund (BK20151017), The Six Major Talent Peak Project of Jiangsu Province (class C, NO WSW-050) and the Young Talents Program of Jiangsu Cancer Hospital (QL201816). Declaration of Interests: The authors stated: None. Ethics Approval Statement: The authors stated: Not applicable.

Ischemia-reperfusion (I/R) injury is a challenging clinical problem, especially injuries involving the gastrointestinal tract. Mitochondrial DNA (mtDNA) is released upon cell death and stress, and can induce the inflammatory response. We aimed to investigate the role of mtDNA in the pathogenesis of intestinal I/R. Intestinal I/R model was established with clamping of the superior mesenteric artery, and IEC-6 cells were incubated under hypoxia/reoxygenation (H/R) conditions to simulate I/R injury. Using in vitro models, H/R up-regulated oxidative stress, disrupted mitochondrial activity and the mitochondrial membrane potential, induced apoptosis and elevated the mtDNA levels in the supernatant of intestinal epithelial cells, and the co-culture of mtDNA with human primary dendritic cells significantly elevated TLR9-MyD88 expression and enhanced the production of inflammatory cytokines and chemokines. MtDNA was also released in a mouse model of intestinal I/R and was associated with the increased secretion of inflammatory cytokines and increased gut barrier injury compared with that of the sham group. We concluded that mtDNA contributes to I/R injury and may serve as a biomarker of intestinal I/R. We further suggest that oxidized mtDNA originated from IECs during intestinal I/R exacerbates the acute proinflammatory process by eliciting the production of proinflammatory cytokines and chemokines.

AbstractRecent studies have implied a prognostic value of the prognostic nutritional index (PNI) in postoperative septic complications of elective colorectal surgeries. However, the evaluation of PNI in contaminated surgeries for gastrointestinal (GI) fistula patients is lack of investigation. The purpose of this study was to explore the predictive value of PNI in surgical site infections (SSIs) for GI fistula patients undergoing bowel resections.A retrospective review of 290 GI patients who underwent intestinal resections between November 2012 and October 2015 was performed. Univariate and multivariate analyses were conducted to identify risk factors for SSIs, and receiver operating characteristic cure was used to quantify the effectiveness of PNI.SSIs were diagnosed in 99 (34.1%) patients, with incisional infection identified in 54 patients (18.6%), deep incisional infection in 13 (4.5%), and organ/space infection in 32 (11.0%). receiver operating characteristic curve analysis defined a PNI cut-off level of 45 corresponding to postoperative SSIs (area under the curve [AUC] = 0.72, 76% sensitivity, 55% specificity). Furthermore, a multivariate analysis indicated that the PNI < 45 [odd ratio (OR): 2.24, 95% confidence interval (CI): 1.09–4.61, P = 0.029] and leukocytosis (OR: 3.70, 95% CI: 1.02–13.42, P = 0.046) were independently associated with postoperative SSIs.Preoperative PNI is a simple and useful marker to predict SSIs in GI fistula patients after enterectomies. Measurement of PNI is therefore recommended in the routine assessment of patients with GI fistula receiving surgical treatment.

Background Recent animal studies have shown that mitochondrial dysfunction initiates and accelerates renal injury in sepsis, but its role in sepsis remains unknown. Mitochondrial stress or dying cells can lead to fragmentation of the mitochondrial genome, which is considered a surrogate marker of mitochondrial dysfunction. Therefore, we evaluated the efficiency of urinary mitochondrial DNA (UmtDNA) as a marker of renal dysfunction during sepsis-induced acute kidney injury (AKI). Methods We isolated DNA from plasma and urine of patients. mtDNA levels were quantified by quantitative PCR. Sepsis patients were divided into no AKI, mild AKI, and severe AKI groups according to RIFLE criteria. Additionally, cecal ligation and puncture (CLP) was established in rats to evaluate the association between UmtDNA and mitochondrial function. Results A total of 52 (49.5%) developed AKI among enrolled sepsis patients. Increased systemic mtDNA did not correlate with systemic inflammation or acute renal dysfunction in sepsis patients, while AKI did not have an additional effect on circulating mtDNA levels. In contrast, UmtDNA was significantly enriched in severe AKI patients compared with that in the mild AKI or no AKI group, positively correlated with plasma creatinine, urinary neutrophil gelatinase-associated lipocalin, and kidney injury molecule-1, and inversely with the estimated glomerular filtration rate. Additionally, UmtDNA increased in rats following CLP-induced sepsis. UmtDNA was predictive of AKI development and correlated with plasma creatinine and blood urea nitrogen in the rat sepsis model. Finally, the UmtDNA level was inversely correlated with the cortical mtDNA copy number and relative expression of mitochondrial gene in the kidney. Conclusion An elevated UmtDNA level correlates with mitochondrial dysfunction and renal injury in sepsis patients, indicating renal mitochondrial injury induced by sepsis. Therefore, UmtDNA may be regarded as a valuable biomarker for the occurrence of AKI and the development of mitochondria-targeted therapies following sepsis-induced AKI.

Surgical site infection (SSI) is the most common complication following surgical procedures. This study aimed to determine risk factors associated with SSI in patients with Crohn’s disease (CD) complicated with gastrointestinal fistula.

Surgical site infection presents as a significant problem that limits the potential benefits of surgical interventions. This study is to investigate risk factors for postoperative SSI in patients with Crohn’s disease receiving definitive bowel resection. A case-control study including 49 patients with SSI and 105 patients without SSI was performed. Demographics, clinical characteristics, laboratory information, medical and surgical data were compared between groups. Significant elements were subsequently brought into logistic regression analysis for further identification. Patients with SSI exhibited higher tobacco usage rate (p = 0.03), lower preoperative hemoglobin (p = 0.02) and pre-albumin level (p = 0.02). Bowel penetration instead of stricture was more frequent in patients with SSI (p = 0.04). Longer duration of operation (p = 0.03) and higher intraoperative lactate level (p = 0.02) were observed in patients with SSI. Logistic analysis identified that preoperative pre-albumin (95% CI: 0.2~0.7; OR = 0.5; p = 0.03), duration of operation (95% CI: 2.3~9.5; OR = 3.8; p = 0.03) and intraoperative lactate level (95% CI: 1.7~7.2; OR = 3.4; p = 0.04) were associated with postoperative surgical site outcome. Our data has identified that lower preoperative pre-albumin, longer duration of operation and higher intraoperative lactate level are risk factors for SSI in patients with Crohn’s disease receiving definitive bowel resection.

BACKGROUND Diabetes mellitus (DM) is a critical medical problem that can make people more likely to develop infectious complications, even sepsis. However, the influence of DM on the outcomes of septic patients is still controversial. Thus, we conducted the present meta-analysis to investigate whether DM worsens outcomes of septic patients. MATERIAL AND METHODS We searched studies from PubMed, Embase, and Cochrane Library databases from 1966 to July 1, 2016. The primary outcome we chose was 28-day or 30-day mortality or in-hospital mortality. RESULTS Our meta-analysis of 10 enrolled studies performed between 2000 and 2016 shows that the mortality rate of septic patients with DM was slightly lower than that of non-diabetic patients (risk ratio [RR]=0.97, 95% confidence interval [CI]: 0.96 to 0.98, P<0.00001). On the other hand, septic patients with DM had a shorter hospital stay (weighted mean difference (WMD)=-2.27, 95% CI: -4.11 to -0.44, P=0.01), a higher incidence rate of AKI (RR=1.56, 95% CI: 1.25 to 1.95, P<0.001), and a similar incidence of respiratory dysfunction (RR=0.86, 95% CI: 0.71 to 1.04, P=0.11) compared with those without DM. CONCLUSIONS The results from the meta-analysis suggest that DM does not impair the outcome of patients with sepsis, and the incidence of acute kidney injury increases dramatically in septic patients with DM. Due to the limitations of the analysis, more well-designed trials are still necessary.

Inflammatory bowel disease (IBD), particularly Crohn's disease, frequently causes intestinal fibrosis that ultimately leads to formation of strictures requiring bowel resection. Currently there is no effective antifibrotic therapy available for this disease. Pirfenidone is a small compound that has a broad spectrum of antifibrogenic effect and has been used for the treatment of fibrotic diseases in various organs. The present study aimed to investigate the antifibrogenic effect of pirfenidone in a dextran sulfate sodium (DSS)-induced murine colitis model. C57BL/6 mice were used and animals were randomly divided into groups receiving pirfenidone or vehicle by oral or transanal routes. Inflammation- and fibrosis-related indexes including body weight, colon length, disease activity, histological change, mRNA expression of pro-inflammatory and pro-fibrogenic cytokines were assessed. Furthermore, we performed in vitro analysis using CCD18-Co fibroblasts to evaluate cell proliferation, transdifferentiation, and viability after the cells were cultured with pirfenidone. It was found that oral administration of pirfenidone reduced deposition of collagen in colitis-associated fibrosis, and significantly suppressed the mRNA expression of col1a2, col3a1, and TGF-β. Moreover, pirfenidone inhibited the activation of TGF-β-related smad and MAPK pathways both in vitro and in vivo. Clinical and histological evaluation demonstrated that pirfenidone had no anti-inflammatory effect. The antifibrogenic effect was reduced when pirfenidone was administered in a delayed manner and was unobserved if given locally. Pirfenidone suppressed fibroblast proliferation and transdifferentiation without observed toxicity. Altogether, our results suggested that oral pirfenidone protects against fibrosis of DSS-induced colitis through inhibiting the proliferation of colonic fibroblasts and TGF-β signaling pathways.

Polypropylene mesh, as a temporary abdominal closure device, may cause mechanical intestine injury and inflammatory response. Chitosan/gelatin hydrogel has excellent biocompatibility, soft and elastic properties. This work is to assess the effects of the chitosan/gelatin hydrogel coated polypropylene mesh on open abdomen wounds. Histological analysis and detection of healing-related factors were conducted to evaluate the inflammation and wound healing process. After 1-day implantation in a murine model of open abdomen, the coated polypropylene mesh, compared with simple polypropylene mesh, demonstrated well protection of the intestine serosa. After 14-day implantation, it reduced the inflammation response by down-regulating the cytokines interleukin-6 and tumor necrosis factor-α, and up-regulating the anti-inflammatory factor interleukin-10. Meanwhile, the composite stimulated granulation tissue growth, and promoted matrix deposition and angiogenesis after 7 and 14 days. In conclusion, the modified temporary abdominal closure composite could significantly protect the intestines from mechanical damage and accelerate wound healing.