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Internal organs heal injuries with new connective tissue, but the cellular and molecular events of this process remain obscure. By tagging extracellular matrix around the mesothelium lining in mouse peritoneum, liver and cecum, here we show that preexisting matrix was transferred across organs into wounds in various injury models. Using proteomics, genetic lineage-tracing and selective injury in juxtaposed organs, we found that the tissue of origin for the transferred matrix likely dictated the scarring or regeneration of the healing tissue. Single-cell RNA sequencing and genetic and chemical screens indicated that the preexisting matrix was transferred by neutrophils dependent on the HSF–integrin AM/B2-kindlin3 cascade. Pharmacologic inhibition of this axis prevented matrix transfer and the formation of peritoneal adhesions. Matrix transfer was thus an early event of wound repair and provides a therapeutic window to dampen scaring across a range of conditions.Rinkevich and colleagues show that preexisting matrix is transferred by neutrophils across organs into injured sites in a manner dependent on integrin activation.

The classical view of the immune system has changed by the discovery of novel T-helper (Th) subsets, including Th17 (IL-17A-producing cells). IL-17A participates in immune-mediated glomerulonephritis and more recently in inflammatory pathologies, including experimental renal injury. Peritoneal dialysis patients present chronic inflammation and Th1/Th2 imbalance, but the role of the Th17 response in peritoneal membrane damage has not been investigated. In peritoneal biopsies from dialyzed patients, IL-17A immunostaining was found mainly in inflammatory areas and was absent in the healthy peritoneum. IL-17A-expressing cells included lymphocytes (CD4+ and γδ), neutrophils, and mast cells. Elevated IL-17A effluent concentrations were found in long-term peritoneal dialysis patients. Studies in mice showed that repeated exposure to recombinant IL-17A caused peritoneal inflammation and fibrosis. Moreover, chronic exposure to dialysis fluids resulted in a peritoneal Th17 response, including elevated IL-17A gene and protein production, submesothelial cell infiltration of IL-17A-expressing cells, and upregulation of Th17 differentiation factors and cytokines. IL-17A neutralization diminished experimental peritoneal inflammation and fibrosis caused by chronic exposure to dialysis fluids in mice. Thus, IL-17A is a key player of peritoneum damage and it may be a good candidate for therapeutic intervention in peritoneal dialysis patients.

Objective Peritoneal injury is a common complication during totally extraperitoneal inguinal hernia repair, potentially affecting surgical outcomes and patient recovery. Identifying risk factors associated with peritoneal injury is crucial to improving surgical techniques and optimizing patient care. Methods This retrospective study analyzed data from 334 patients who underwent totally extraperitoneal inguinal hernia repair between August 2019 and April 2024. Patients were divided into two groups based on the occurrence of peritoneal injury: injury group (n = 69) and noninjury group (n = 265). Univariate and multivariate logistic regression analyses identified independent risk factors for peritoneal injury. A predictive nomogram was constructed using significant variables from the multivariate analysis. The performance of the nomogram was evaluated using the area under the receiver operating characteristic curve (AUC), calibration plots, and decision curve analysis. Results Peritoneal injury occurred in 20.7% of the cases. Multivariate analysis identified the following five independent risk factors: anatomical misrecognition (odds ratio: 7.55; p = 0.005), insufficient peritoneal tension (odds ratio: 2.95; p = 0.007), hernial sac diameter ≥4 cm (odds ratio: 2.75; p = 0.008), prior infraumbilical surgery (odds ratio: 2.50; p = 0.021), and use of sharp medial hernia sac dissection techniques (odds ratio: 5.20; p = 0.006). Body mass index was a significant factor in univariate analysis (p = 0.004) but not in multivariate analysis (p = 0.180). The nomogram demonstrated good discriminative ability (AUC = 0.841) and calibration. The decision curve analysis indicated that the nomogram provided clinical utility across a range of threshold probabilities. Conclusions The study identified key risk factors for peritoneal injury during totally extraperitoneal inguinal hernia repair and developed a predictive nomogram with strong discriminative ability. Awareness of these factors enables surgeons to preoperatively stratify risk based on imaging-assessed hernia characteristics and patient history, thereby guiding technique selection.

Background Conventional laparoscopic surgery uses CO 2 that is dry and cold, which can damage peritoneal surfaces. It is speculated that disseminated cancer cells may adhere to such damaged peritoneum and metastasize. We hypothesized that insufflation using humidified-warm CO 2 , which has been shown to reduce mesothelial damage, will also ameliorate peritoneal inflammation and tumor cell implantation compared to conventional dry-cold CO 2 . Methods Laparoscopic insufflation was modeled in mice along with anesthesia and ventilation. Entry and exit ports were introduced to maintain insufflation using dry-cold or humidified-warm CO 2 with a constant flow and pressure for 1 h; then 1000 or 1 million fluorescent-tagged murine colorectal cancer cells (CT26) were delivered into the peritoneal cavity. The peritoneum was collected at intervals up to 10 days after the procedure to measure inflammation, mesothelial damage, and tumor burden using fluorescent detection, immunohistochemistry, and scanning electron microscopy. Results Rapid temperature control was achieved only in the humidified-warm group. Port-site tumors were present in all mice. At 10 days, significantly fewer tumors on the peritoneum were counted in mice insufflated with humidified-warm compared to dry-cold CO 2 ( p  < 0.03). The inflammatory marker COX-2 was significantly increased in the dry-cold compared to the humidified-warm cohort ( p  < 0.01), while VEGFA expression was suppressed only in the humidified-warm cohort. Significantly less mesothelial damage and tumor cell implantation was evident from 2 h after the procedure in the humidified-warm cohort. Conclusions Mesothelial cell damage and inflammation are reduced by using humidified-warm CO 2 for laparoscopic oncologic surgery and may translate to reduce patients’ risk of developing peritoneal metastasis.

Patients undergoing long‐term peritoneal dialysis (PD) frequently develop peritoneal fibrosis and angiogenesis, leading to membrane dysfunction. Transglutaminase 2 (TG2) stabilizes the extracellular matrix against proteases. In an animal model, inhibition of TG2 reduced peritoneal fibrosis, angiogenesis, and inflammation. We investigated the expression of TG2 in 163 human peritoneal membrane tissue samples, including controls, tissues exposed to conventional acidic or low‐glucose degradation product (GDP) pH‐neutral solutions, and those with peritonitis or encapsulating peritoneal sclerosis (EPS), and explored the role of TG2 in high‐glucose–induced pathophysiology in mesothelial cells. TG2 expression was upregulated in association with peritoneal membrane injury and was the highest in peritonitis. TG2 expression was correlated with peritoneal membrane thickness, CD68‐positive macrophages, and myofibroblast expression. TG2 was expressed in mesothelial cells, α‐smooth muscle actin‐positive myofibroblast expression, macrophages, and endothelial cells in the diseased state. In cultured mesothelial cells, high‐glucose–induced upregulation of collagen 1, TGF‐β1, and TG2 was suppressed by a TG2 inhibitor or by TGF‐β1 small interfering RNA. TG2 is involved in the development of peritoneal injury during PD. High‐glucose dialysate is involved in the induction of peritoneal fibrosis through the interactive regulation of TGF‐β and TG2. Targeting TG2 may offer therapeutic potential for managing PD complications and EPS.

Peritoneal tear during endoscopic extraperitoneal inguinal hernioplasty (TEP) results in pneumoperitoneum and loss of extraperitoneal space. To avoid bowel adhesions, internal herniation, and mesh migration, closure of the peritoneal opening is preferred. The present study was conducted to evaluate the efficacy of various operative techniques for the closure of peritoneal laceration. Between April 2000 and May 2001, 100 consecutive patients undergoing 123 TEPs were recruited for the present study. The incidence of peritoneal tear and techniques for the closure of peritoneal opening were documented. Operative time and postoperative morbidity were compared among groups for which different closure methods of peritoneal laceration were used. The incidence of peritoneal tear was 47%. The mean operative times of unilateral TEPs with and without peritoneal laceration were 66 min and 53 min, respectively (p<0.05). Techniques for the closure of the peritoneal opening included endoscopic stapling (n = 12), endoscopic suturing (n = 14), and pretied suture loop ligation (n = 21). The mean operative times for unilateral TEPs with endoscopic stapling, pretied suture loop ligation, and endoscopic suturing of peritoneal tear were 53, 64, and 82 min, respectively (p<0.05). Comparison of postoperative morbidity showed no significant differences among the three groups. Peritoneal tear is a frequent and challenging intraoperative event during TEP. Its occurrence significantly prolongs the length of operation. Endoscopic stapling and pretied suture loop ligation are safe and quick techniques for the closure of peritoneal tear during TEP.

The genetic predisposition to high glucose‐induced peritoneal membrane (PM) injury during peritoneal dialysis (PD) and its mechanisms are of substantial clinical interest. We compared PD‐induced peritoneal injury between two closely related mouse substrains, C57BL/6J and C57BL/6N, which differ in the function of the mitochondrial enzyme nicotinamide nucleotide transhydrogenase (NNT). Nnt (+/+) C57BL/6N mice exhibited significantly greater susceptibility, as indicated by mesothelial cell loss, fibrosis, neoangiogenesis, inflammation, M1 macrophage infiltration, and reduced ultrafiltration. To further investigate NNT's role, we silenced NNT in vitro. Knockdown prevented mitochondrial ROS accumulation, reduced pro‐inflammatory mediator release in mesothelial cells, inhibited M1 polarization in macrophages, and impaired fibroblast proliferation under high glucose. We also observed a reverse NNT reaction in fibroblasts, contributing to glucose‐induced ROS. Our findings indicate reduced genetic susceptibility of Nnt (−/−) C57BL/6J mice to PD‐induced PM damage and identify NNT as a potential therapeutic target for PD‐associated peritoneal injury.

Background High-intensity ultrasound (HIUS) has been increasingly investigated as a possible tool in the treatment of multiple tumor entities. However, there is only little knowledge on the effect of HIUS on the peritoneum. This preliminary study aims to investigate HIUS’ potential for altering the peritoneal surface and potentially improving current treatments for peritoneal metastases. For this purpose, HIUS’ qualitative and quantitative structural effects on the peritoneal tissue were analyzed by means of light, fluorescence and electron microscopy. Methods Proportional sections were cut from the fresh postmortem swine peritoneum. Peritoneal surfaces were covered with a 6 mm thick liquid film of 0.9% NaCl. HIUS was applied in all tissue samples for 0 (control), 30, 60, 120 and 300 s. Peritoneal tissues were analyzed using light-, fluorescence and electron microscopy to detect possible structural changes within the tissues. Results Following HIUS, a superficial disruption of peritoneal tissue was visible in light microscopy, which amplified with increased time of HIUS’ application. Fluorescence microscopy showed both peritoneal and subperitoneal disruption with tissue gaps. Electron microscopy revealed structural filamentation of the peritoneal surface. Conclusion Our data indicate that HIUS causes a wide range of effects on the peritoneal tissue, including the formation of small ruptures in both peritoneal and subperitoneal tissues. However, according to our findings, these disruptions are limited to a microscopical level. Further studies are required to evaluate whether HIUS application can benefit current therapeutic regimens on peritoneal metastases and possibly enhance the efficacy of intraperitoneal chemotherapy.

The current literature and guidelines recommend that determination of peritoneal violation is done first in cases of anterior abdominal stab wounds. The primary endpoint of this study was to determine the reliability of computed tomographic (CT) tractography to assess peritoneal violation in anterior abdominal stab wounds. The secondary endpoint is to compare local wound exploration between conventional CT and CT tractography in the evaluation of peritoneal violation. A total of 252 patients who were referred with anterior abdominal stab wounds were included in this prospective observational study. Three techniques (local wound exploration, conventional abdominal tomography, and CT tractography) were used to evaluate peritoneal violation. Sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), and accuracy were calculated for each technique to determine peritoneal violation. The results for the local wound exploration were 100% sensitivity, 100% specificity, 100% PPV, 100% NPV, and 100% accuracy. The results for CT tractography were 95% sensitivity, 100% specificity, 100% PPV, 80% NPV, and 96% accuracy. Conventional abdominal tomography results were 87% sensitivity, 50% specificity, 91% PPV, 40% NPV, and 82% accuracy. Local wound exploration is 100% effective in determining peritoneal violation with anterior abdominal stab wounds. CT tractography is better than conventional CT in detecting peritoneal violation. However, we do not recommend CT tractography in anterior abdominal stab wounds due to the false-negative results.

The increasing use of laparoscopic surgery for advanced gastrointestinal cancer raises concerns about intra-peritoneal tumor spread. Prevention of peritoneal dissemination is extremely important but a preventive modality is lacking. The aim of this study was to examine a novel approach (hyperthermic CO2 insufflation, HT-CO2) for preventing peritoneal dissemination during laparoscopic surgery. A peritoneal dissemination model was established in Balb/c nu/nu mice by intraperitoneal injection of human colon cancer cells (SW1116, 1×106). The mice (n = 48) were subsequently randomized into two groups and subjected to hyperthermic CO2 (43°C, >95% humidity, HT-CO2 group) or standard normothermic CO2 (21°C, <1% relative humidity, NT-CO2 group) insufflation for 3 hours. The mice were sacrificed 28 days later. The peritoneal dissemination was quantitatively analyzed by counting and weighing the peritoneal nodules. The port sites and ascites volume were measured. The peritoneal damage of HT-CO2 was histologically examined with light microscopy and scanning electron microscopy. Intra-abdominal adhesions were evaluated 4 weeks later. The number of peritoneal nodules in the HT-CO2 group was significantly less than that in the NT-CO2 group (10.21±3.72 vs. 67.12±5.49, P<0.01). The mean weight of metastatic tumors in the HT-CO2 group was significantly lower than that in the NT-CO2 group (0.31±0.10g vs. 2.16±0.31g, P<0.01). Massive ascites were found in the NT-CO2 group while significantly less ascites developed in HT-CO2- treated mice (8.26±0.31ml vs. 1.27±0.28ml, P<0.01). No port-site metastases were detected in the HT-CO2 group while the incidence of the NT-CO2 group was 12.5% (3/24). HT-CO2 subjection resulted in slight peritoneal damage; the peritoneum returned to normal within five days. No adhesions formed after HT-CO2 treatment. HT-CO2 can suppress peritoneal dissemination of colon cancer cells and only causes slight and transient peritoneal damage. HT-CO2 may serve as a promising adjuvant treatment for preventing peritoneal dissemination in laparoscopic resection of advanced colorectal cancer.