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The pathogenesis of endometriosis remains unclear. Endometrial cells in retrograde menstruation are considered the source of endometriosis; therefore, we hypothesized that the eutopic endometrium may provide clues regarding the pathogenesis. We aimed to clarify the role of eutopic endometrial cells in endometriosis development.Eutopic endometrial tissues were obtained from patients with or without endometriosis, and expression of cell surface molecules in eutopic endometrial stromal cells (ESCs) was evaluated via iTRAQ-based proteomic analysis. Based on the results, we focused on galectin-3. Galectin-3 expression in clinical samples was confirmed by immunohistochemistry and Western blot analysis. The concentration of secreted galectin-3 was measured using enzyme-linked immunosorbent assays. Adhesion and migration of ESCs were evaluated by in vitro adhesion and wound healing assays. The cytotoxicity of natural killer cells was measured via calcein release assays. Cell proliferation was measured using the CyQUANT Cell Proliferation Assay Kit.iTRAQ analysis revealed that galectin-3 expression was specifically elevated in the ESCs from endometriosis patients. Immunohistochemistry confirmed galectin-3 overexpression in the eutopic endometrium of endometriosis, irrespective of the menstrual phase. Galectin-3 was overexpressed and secreted by the eutopic ESCs from patients with endometriosis compared to that from patients without endometriosis. Galectin-3 expression in ESCs increased adhesion and migration, whereas galectin-3 inhibitors impaired these processes. Galectin-3 reduced the cytotoxicity of natural killer cells toward ESCs, while not affecting cell proliferation.Galectin-3 promotes peritoneal engraftment of ESCs due to impaired immune surveillance in the peritoneal cavity and increases ESCs adhesion and migration to the peritoneum.

The author suggests differentiating the notions "the location of organs in relation to the peritoneum" and "coverage of organs with the peritoneum". According to the author, all the organs, except the ovaries, are located extraperitoneally but are covered on one, three or all sides., Предлагается различать понятия "расположение органов по отношению к брюшине" и "покрытие органов брюшиной". Все органы, за исключением яичников, расположены экстраперитонеально, но покрыты брюшиной с одной, с трех или со всех сторон., Пропонується розрізняти поняття "розміщення органів по відношенню до очеревини" і "покриття органів очеревиною". На думку автора, всі органи, за винятком яєчників, розміщені екстраперитонеально, але покриті очеревиною з однієї, з трьох або з усіх боків.

The safe establishment of pneumoperitoneum is a critical step in all laparoscopic surgeries. A closed pneumoperitoneum is usually obtained by inserting a Veress needle into the peritoneal cavity. However, there is no definite measure to visually confirm the position of the Veress needle tip inside the peritoneal cavity. This study aimed to describe a method of real-time visual detection of peritoneal placement of the Veress needle using an incorporated optical coherence tomography (OCT) probe in a porcine model. A 14-gauge Veress needle was incorporated with a miniature fiber probe to puncture the piglet’s abdominal wall into the peritoneal cavity. A total of 80 peritoneal punctures were attempted in four piglets. For each puncture, continuous two-dimensional OCT images of the abdominal wall were acquired for real-time visual detection of the needle placement into the peritoneal cavity. Characteristic OCT image patterns could be observed during the puncturing process, especially a deep V-shaped concave pattern before the peritoneum puncture, which was a crucial feature. A statistical difference in the OCT signal standard deviation value also indicated the differentiability of images between the peritoneum and extra-peritoneal tissue layers. A success rate of 97.5% could be achieved with the guidance of the OCT images. OCT images translate the blind closed technique of peritoneal access into a visualized procedure, thus improving peritoneal access safety.

Peritoneal dialysis (PD) is performed by filling the peritoneal cavity with dialysis fluid, allowing this to dwell before draining the fluid out and repeating the process with fresh dialysate. Solute transfer is by diffusion and convection transport whilst water moves across the osmotic or oncotic gradient.

Ascites is a pathological accumulation of fluid in the peritoneal cavity due to various etiologies, often associated with renal failure. Paracentesis is a simple method of removing ascitic fluid by inserting a needle into the peritoneal cavity, often performed at the patient's bedside. It can be both diagnostic and therapeutic. Ultrasound imaging allows the diagnosis of ascites, the identification of the puncture site on the abdominal wall during the pre-procedural phase, the real time evaluation of the needle and the continuous course of the maneuver. This eco-guide technique has higher effectiveness and lower risk of complications than the "blind" venipuncture technique. Ultrasound-guided paracentesis, when performed by nephrologists, reduces the waiting time both for the execution of paracentesis and for the diagnosis, treatment and follow-up of ascites.

Intestinal parasitic nematodes affect a quarter of the world’s population, typically eliciting prominent effector Th2-driven host immune responses. As not all infected hosts develop protection against reinfection, our current understanding of nematode-induced memory Th2 responses remains limited. Here, we investigated the activation of memory Th2 cells and the mechanisms driving early recall responses to the enteric nematode Heligmosomoides polygyrus in mice. We show that nematode-cured mice harbor memory Th2 cells in lymphoid and non-lymphoid organs with distinct transcriptional profiles, expressing recirculation markers like CCR7 and CD62-L in the mesenteric lymph nodes (mLN), and costimulatory markers like Ox40, as well as tissue homing and activation markers like CCR2, CD69 and CD40L in the gut and peritoneal cavity (PEC). While memory Th2 cells persist systemically in both lymphoid and non-lymphoid tissues following cure of infection, peritoneal memory Th2 cells in particular displayed an initial prominent expansion and strong parasite-specific Th2 responses during early recall responses to a challenge nematode infection. This effect was paralleled by a significant influx of dendritic cells (DC) and eosinophils, both also appearing exclusively in the peritoneal cavity of reinfected mice. In addition, we show that within the peritoneal membrane lined by peritoneal mesothelial cells (PeM), the gene expression levels of cell adhesion markers VCAM-1 and ICAM-1 decrease significantly in response to a secondary infection. Overall, our findings indicate that the host peritoneal cavity in particular harbors prominent memory Th2 cells and appears to respond directly to H. polygyrus by an early recall response via differential regulation of cell adhesion markers, marking the peritoneal cavity an important site for host immune responses to an enteric pathogen.

The instillation of local anesthetic into the peritoneal cavity at the time of various types of laparoscopic surgery has been found to improve postoperative pain as quantified by decreased time to discharge, decreased pain severity scores, and decreased amounts of rescue narcotic. No significant safety issues have been identified with the practice of intraperitoneal instillation of local anesthetic. Dosage, placement location and timing of local anesthetic administration has been evaluated in a variety of settings, for different procedures and prior to and after dissection. Although more research is needed to standardize the practice of intraperitoneal local anesthetic use, it has been demonstrated as helpful as an adjunct in managing the pain associated with laparoscopic surgery and should be considered for all patients undergoing laparoscopic surgery.

The model flatworm Mesocestoides vogae proliferating stage of infection elicits immunosuppression in the host. It was used to investigate the effects of human leukocyte extract (DLE) alone and in combination with anthelmintic albendazole (ABZ) on the reduction in peritoneal infection, peritoneal exudate cells (PECs), their adherent counterparts, and peritoneal exudates after the termination of therapy. Balb/c mice were infected with the larvae of M. vogae. PECs and adherent macrophages were studied via flow cytometry, mRNA transcript levels, and immunofluorescence. The cytokine levels were measured via ELISA and larvae were counted. ABZ significantly reduced larval counts (581.2 ± 65, p < 0.001), but the highest reduction was observed after combined treatment with ABZ and DLE (389.2 ± 119, p < 0.001) in comparison with the control. Compared to an infected group, the proportions of CD11b+CD19- myeloid cells with suppressive ability decreased after albendazole (ABZ) in combination with DLE, which was the most effective in the elevation of B cells and CD11b+F4/80mid/highMHCIIhigh macrophages/monocytes (22.2 ± 5.4%). Transcripts of the M2 macrophage markers (arginase 1, FIZZ-1, and Ym-1) were downregulated after DLE and combined therapy but not after ABZ, and the opposite trend was seen for iNOS. This contrasts with reduced ex vivo NO production by LPS-stimulated PECs from DLE and ABZ+DLE groups, where adherent macrophages/monocytes had elevated transcripts of the INF-γ receptor and STAT1 and reduced expression of STAT3, STAT6, and IL-10. Each therapy differentially modulated transcription profiles and concentrations of IFN-γ, TNF-α, IL-12p40, IL-6, IL-10, and TGF-β cytokines. DLE strongly ameliorated ABZ-induced suppression of INF-γ and IL-12 and preserved downregulation for IL-4, IL-10, and TGF-β. Epigenetic study on adherent macrophages from infected mice showed that ABZ, ABZ-sulfoxide, and DLE could interact with the mRNA of examined markers in a dose-dependent pattern. Co-administration of DLE with ABZ seemed to augment the drug’s larvicidal effect via modulation of immunity. In comparison with ABZ, combined therapy was the most effective in alleviating parasite-induced Th2/Treg/STAT3/STA6 directed immunosuppression by stimulating the Th1 cytokines, M1 macrophage polarization, and activation of the IFNγ/STAT1 signaling pathway.

INTRODUCTION. Diffuse peritonitis remains a topical problem of modern medicine and is still associated with high mortality. The OBJECTIVE of this work was to develop an objective and easy-to-perform method for determining the indications for programmed relaparotomy in patients with diffuse peritonitis on the basis of determining the aggressiveness of its course.MATERIAL AND METHODS. The work was based on the results of treatment of 100 patients with diffuse peritonitis. Depending on the pH of the exudate of the peritoneal cavity, the patients were divided into 2 groups. The first group consisted of patients with pH value of peritoneal exudate more than 6.2 (75 patients), and the second group consisted of patients with pH value of peritoneal exudate 6.2 and less (25 patients).RESULTS. As a result of the treatment in group I, the mortality rate was 12.0 %. In group II, the mortality rate was 56.0 %. The difference was statistically significant (pCONCLUSION. We concluded that at pH value of exudate 6.2 or less and the absence of obvious clinical improvement, the patient had been showed to performance the programmed remedial relaparotomy no later than 48 hours from the first operation.The authors declare no conflict of interest.The authors confirm that they respect the rights of the people participated in the study, including obtaining informed consent when it is necessary, and the rules of treatment of animals when they are used in the study. Author Guidelines contains the detailed information.

External genital endometriosis is an inflammatory, estrogen-dependent disease that develops predominantly in women of reproductive age and is characterized by the presence of pain syndrome and infertility. Today, endometriosis is one of the most common gynecological diseases in women of reproductive age, however, the etiology and pathogenesis of it are not completely clear. Violations of systemic immunity are most important in the pathogenesis of endometriosis. The literature data on the features of the immune response in endometriosis in combination with genital infection are few and contradictory. Purpose – to study the features of systemic immunity in women with external genital endometriosis and pathogens of genital infection.A total of 159 women with external genital endometriosis were examined. The main lymphocyte subpopulations, the functional activity of neutrophils and peripheral blood monocytes, and the content of cytokines in the blood serum were studied. A study of systemic immunity was performed in women with 1-2 and 3-4 stages of endometriosis, as well as depending on the presence of pathogens of genital infection. The presence of Chlamydia trachomatis, Ureaplasma spp., Mycoplasma genitalium, HSV1, 2/CMV, HPV in the endometrium, peritoneal fluid, and endometrioid heterotopies was determined. Statistical processing was performed using the IBM SPSS Statistics Version 22.2 statistical analysis software package.According to the results of the study, it was found that women with endometriosis of stages 1-2 show signs of systemic inflammation with a predominance of the Th2 type of immune response and inhibition of cellular immunity. A particular feature of HPV was an increase in T-NK lymphocytes, a decrease in IL-2 and neutrophil functional activity. The presence of Ureaplasma spp./Mycoplasma genitalium was characterized by a decrease in cellular immunity and an increase in T-NK cells. Only with HPV and Ureaplasma spp./Mycoplasma genitalium decreased synthesis of IL-2, IL-6. With 3-4 stages, the most significant changes in immunity were found in groups of women with genital infection. When HPV – a high level of IgA, increased IgM, IL-8. With Ureaplasma spp./Mycoplasma genitalium – inhibition of cellular immunity, high levels of IgA, reduction of neutrophil phagocytic activity.Thus, in women with endometriosis in the presence of pathogens of genital infection revealed features that may contribute to the development and progression of the disease.

Macrophages play an important role in the inflammatory response. Their various biological functions are induced by different membrane receptors, including Toll-like receptors, which trigger several intracellular signaling cascades and activate the inflammasomes, which in turn elicit the release of inflammatory mediators such as cytokines. In this study, we present a novel method for the isolation of human mature peritoneal macrophages. This method can be easily implemented by gynecologists who routinely perform laparoscopy for sterilization by tubal ligation or surgically intervene in benign gynecological pathologies. Our method confirms that macrophages are the main peritoneal leukocyte subpopulation isolated from the human peritoneum in homeostasis. We showed that primary human peritoneal macrophages present phagocytic and oxidative activities, and respond to activation of the main proinflammatory pathways such as Toll-like receptors and inflammasomes, resulting in the secretion of different proinflammatory cytokines. Therefore, this method provides a useful tool for characterizing primary human macrophages as control cells for studies of molecular inflammatory pathways in steady-state conditions and for comparing them with those obtained from pathologies involving the peritoneal cavity. Furthermore, it will facilitate advances in the screening of anti-inflammatory compounds in the human system.

Abdominal pregnancy is a type of ectopic pregnancy where the gestational sac is implanted in the peritoneal cavity. It may be either a primary or a secondary abdominal pregnancy. Secondary abdominal pregnancies result due to early rupture of tubal ectopic pregnancy into the peritoneal cavity. Here we present a case of 28 year old G3P2L2 who presented to our hospital with secondary abdominal pregnancy with a dead fetus.

Purpose In advanced gastric cancer, peritoneal dissemination is a life‐threatening mode of metastasis. Since the treatment options with conventional chemotherapy remain limited, any novel therapeutic strategy that could control such metastasis would improve the outcome of treatment. We recently developed a unique RNA interference therapeutic regimen (DFP‐10825) consisting of short hairpin RNA against thymidylate synthase (TS shRNA) and cationic liposomes. The treatment with DFP‐10825 has shown remarkable antitumor activity in peritoneally disseminated human ovarian cancer–bearing mice via intraperitoneal administration. In this study, we expanded DFP‐10825 to the treatment of peritoneally disseminated gastric cancer. Methods DFP‐10825 was administered intraperitoneally into mice with intraperitoneally implanted human gastric cancer cells (MKN45 or NCI‐N87). Antitumor activity and host survival benefits were monitored. Intraperitoneal distribution of fluorescence‐labeled DFP‐10825 was monitored in this MKN45 peritoneally disseminated mouse model. Results Intraperitoneal injection of DFP‐10825 suppressed tumor growth in two peritoneally disseminated cancer models (MKN45 and NCI‐N87) and increased the survival time of the MKN45 model without severe side effects. Throughout the treatment regimen, no significant body weight loss was associated with the administration of DFP‐10825. Interestingly, after intraperitoneal injection, fluorescence‐labeled DFP‐10825 retained for more than 72 hours in the peritoneal cavity and selectively accumulated in disseminated tumors. Conclusions Intraperitoneal injection of DFP‐10825 demonstrated effective antitumor activity without systemic severe adverse effects via the selective delivery of RNAi molecules into disseminated tumors in the peritoneal cavity. Our current study indicates that DFP‐10825 could become an alternative option to improve the outcomes of patients with peritoneally disseminated gastric cancer., Intraperitoneal DFP‐10825 showed effective antitumor activity in peritoneally disseminated human gastric cancer–bearing mice. As an alternative treatment regimen, DFP‐10825 has the potential to improve the outcomes of patients with peritoneally disseminated gastric cancer.

T-bet(+) B cells have emerged as a major B cell subset associated with both protective immunity and immunopathogenesis. T-bet is a transcription factor associated with type I adaptive immune response to intracellular pathogens, driving an effector program characterized by the production of IFNγ. Murine infection with the intracellular bacterium, E. muris, generates protective extrafollicular T cell-independent T-bet(+) IgM-secreting plasmablasts, as well as T-bet(+) IgM memory cells. Although T-bet is a signature transcription factor for this subset, it is dispensable for splenic CD11c(+) memory B cell development, but not for class switching to IgG2c. In addition to the T-bet(+) plasmablasts found in the spleen, we show that antibody secreting cells can also be found within the mouse peritoneal cavity; these cells, as well as their CD138-negative counterparts, also expressed T-bet. A large fraction of the T-bet(+) peritoneal B cells detected during early infection were highly proliferative, expressed CXCR3 and CD11b, but unlike in the spleen, they did not express CD11c. T-bet(+) CD11b(+) memory B cells were the dominant B cell population in the peritoneal cavity at 30 days post-infection, and although they expressed high levels of T-bet, they did not require B cell-intrinsic T-bet expression for their generation. Our data uncover a niche for T-bet(+) B cells within the peritoneal cavity during intracellular bacterial infection, and identify this site as a reservoir for T-bet(+) B cell memory.

Intestinal parasitic nematodes affect a quarter of the world's population, typically eliciting prominent effector Th2-driven host immune responses. As not all infected hosts develop protection against reinfection, our current understanding of nematode-induced memory Th2 responses remains limited. Here, we investigated the activation of memory Th2 cells and the mechanisms driving early recall responses to the enteric nematode

Malignant ascites is an abnormal accumulation of fluid within the peritoneal cavity, caused by metastasis of several types of cancers, including colorectal cancer (CRC). Cancer cells in ascites reflect poor prognosis and serve as a good specimen to study tumour heterogeneity, as they represent a collection of multiple metastatic sites in the peritoneum. In the present study, we have employed single-cell RNA-sequencing (scRNA-seq) to explore and characterise ascites-derived cells from a CRC patient. The samples were prepared using mechanical and enzymatic dissociations, and obtained before and after a chemotherapy treatment. Unbiased clustering of 19,653 cells from four samples reveals 14 subclusters with unique transcriptomic patterns in four major cell types: epithelial cells, myeloid cells, fibroblasts, and lymphocytes. Interestingly, the percentages of cells recovered from different cell types appeared to be influenced by the preparation protocols, with more than 90% reduction in the number of myeloid cells recovered by enzymatic preparation. Analysis of epithelial cell subpopulations unveiled only three out of eleven subpopulations with clear contraction after the treatment, suggesting that the majority of the heterogeneous ascites-derived cells were resistant to the treatment, potentially reflecting the poor treatment outcome observed in the patient. Overall, our study showcases highly heterogeneous cancer subpopulations at single-cell resolution, which respond differently to a particular chemotherapy treatment. All in all, this work highlights the potential benefit of single-cell analyses in planning appropriate treatments and real-time monitoring of therapeutic response in cancer patients through routinely discarded ascites samples.

Excessive inflammation drives the progression from sepsis to septic shock. Macrophage migration inhibitory factor (MIF) is of interest because MIF promoter polymorphisms predict mortality in different infections, and anti-MIF antibody improves survival in experimental models when administered 8 hours after infectious insult. The recent description of a second MIF superfamily member, D-dopachrome tautomerase (D-DT/MIF-2), prompted closer investigation of MIF-dependent responses. We subjected Mif-/- and Mif-2-/- mice to polymicrobial sepsis and observed a survival benefit with Mif but not Mif-2 deficiency. Survival was associated with reduced numbers of small peritoneal macrophages (SPMs) that, in contrast to large peritoneal macrophages (LPMs), were recruited into the peritoneal cavity. LPMs produced higher quantities of MIF than SPMs, but SPMs expressed higher levels of inflammatory cytokines and the MIF receptors CD74 and CXCR2. Adoptive transfer of WT SPMs into Mif-/- hosts reduced the protective effect of Mif deficiency in polymicrobial sepsis. Notably, MIF-2 lacks the pseudo-(E)LR motif present in MIF that mediates CXCR2 engagement and SPM migration, supporting a specific role for MIF in the recruitment and accumulation of inflammatory SPMs.

There are numbers of leukocytes present in peritoneal cavity, not only protecting body cavity from infection but also contributing to peripheral immunity including natural antibody production in circulation. The peritoneal leukocytes compose unique immune compartment, the functions of which cannot be replaced by other lymphoid organs. Atypical lymphoid clusters, called "milky spots", that are located in visceral adipose tissue omentum have the privilege of immune niche in terms of differentiation, recruitment, and activation of peritoneal immunity, yet mechanisms underlying the regulation are underexplored. In this review, I discuss the emerging views of peritoneal immune system in the contexts of its development, organization, and functions.

Introduction Ventriculoperitoneal shunt (VPS) is the most common procedure used for cerebrospinal fluid (CSF) diversion in hydrocephalus. Over the years, many technical, procedural, and instrument-related advancements have taken place which have reduced the associated complication rates. Shunt block is a very common complication irrespective of the shunt system used. The abdominal end of the shunt tube gets blocked usually due to plugging of omentum onto the shunt catheter. We describe a technique of catheter fixation and placement under vision coupled with omentopexy done laparoscopically to prevent this complication. Materials and Methods This technique was used in 23 patients (11 female, 12 male; range 16–73 years) afflicted with hydrocephalus from June 2016 and December 2019 after obtaining an informed consent, and the outcomes were noted in terms of shunt patency, complications, if any, and the need for revision. Results The median operation time was 90 minutes (range 35–160 minutes). All shunt catheters were still functional after a mean follow-up of 16.5 months (range 1–34 months) and none required revision. Conclusion Laparoscopic placement of shunt tube along with omental folding is a safe and effective technique for salvaging the abdominal end of VPS and may be helpful in reducing shunt blockage.

Congenital chylous ascites (CCA) is a rare condition where there is an accumulation of chyle in the peritoneal cavity. Primary CCA due to dysplastic lymphatics is the most common cause in children. CCA discovered on ventriculopertoneal (VP) shunt insertion following previous myelomeningocele repair has only been described in a single paper before with the authors recommending a VP shunt safe to be sited in the presence of CCA. In this paper, we present a case of CCA in a term neonate with a myelomeningocele and an imperforate anus who underwent the siting of a VP shunt with no adverse effect. We provide an alternative hypothesise suggesting the link between raised intra-abdominal pressure caused by the imperforate anus as the aetiological factor in CCA.

Peritoneal Free Bodies, also known as Peritoneal Loose Bodies (PLBs) are uncommon entities that are usually coincidental findings in operative procedures or routine investigations. Peritoneal Loose Bodies in excess of 5–7 cm (2–3 in.) are exceedingly rare and have been very occasionally reported. It is a general consensus that such bodies result from the torsion, infarction, calcification and sometimes adhesion of the epiploic appendages to structures in the peritoneal cavity. Here, we discuss the case of a 69-year-old Indian man, who presented with vague abdominal discomfort and occasional difficulty in micturition, and upon diagnostic laparoscopy and subsequent laparotomy, a Peritoneal Loose Body of size approximately 7.5 × 7 × 6.5 cm3 was found intra-abdominally. We evaluate here the diagnostic considerations and the probable mode of origin of this body in this presentation. Peritoneal Loose Bodies are usually benign entities, in that most of them are relatively small in size and inconsequential. However, sometimes the larger and much rarer ‘Giant’ Peritoneal Loose Bodies give rise to symptoms, and intervention is required in those cases. It remains the responsibility of the treating surgeon to avoid unnecessary operative procedures, and determine the suitability of each individual patient for the same.

Tissue-resident macrophages (TRMΦ) are important immune sentinels responsible for maintaining tissue and immune homeostasis within their specific niche. Recently, the origins of TRMΦ have undergone intense scrutiny, in which now most TRMΦ are thought to originate early during embryonic development independent of hematopoietic stem cells (HSCs). We previously characterized two distinct subsets of mouse peritoneal cavity macrophages (MΦ) (large and small peritoneal MΦ) whose origins and relationship to both fetal and adult long-term (LT) HSCs have not been fully investigated. In this study, we employ highly purified LT-HSC transplantation and in vivo lineage tracing to show a dual ontogeny for large and small peritoneal MΦ, in which the initial wave of peritoneal MΦ is seeded from yolk sac–derived precursors, which later require LT-HSCs for regeneration. In contrast, transplanted fetal and adult LT-HSCs are not able to regenerate brain-resident microglia. Thus, we demonstrate that LT-HSCs retain the potential to develop into TRMΦ, but their requirement is tissue specific in the peritoneum and brain.

Lumboperitoneal shunting makes it possible to regulate the flow of cerebrospinal fluid by establishing a connection between the thecal sac and the peritoneal cavity. The main indication for lumboperitoneal shunting in children is idiopathic intracranial hypertension, but the technique is also useful in the treatment of postinfectious, posthemorrhagic, and normotensive hydrocephalus, as well as in the treatment of postsurgical pseudomeningocele or leakage of cerebrospinal fluid. This article reviews nine cases treated at our centre to show the normal imaging findings for lumboperitoneal shunts in children and to provide a succinct review of the possible neurological and abdominal complications associated with this treatment.

The ability of Russell's viper (Daboia siamensis) venom (total RVV) and phospholipase A2 (purified PLA2) to induce the local pathological effects were investigated by the local inflammatory events and the release of inflammatory mediators. Both 0.5 μg of total RVV/mouse and 0.15 μg of purified PLA2/mouse were administered via intra-peritoneal injection. After 30 min, 1 h, 2 h, and 4 h incubation time, the peritoneal cavity was flooded with normal saline and the total leukocytes were collected. The eicosanoids (lipid mediators) and the leukocyte expression of cyclooxygenase (COX-1 and COX-2) were investigated by ELISA assay and western blotting, respectively. The amounts of total leukocytes were increased from 30 min to 2 h, then decreased at 4 h, by both total RVV and purified PLA2. Both treatments also induced the expression of COX-2 which was increased at 2 h and then decreased at 4 h, whereas only purified PLA2 induced the expression level of a COX-1 protein which was increased at 30 min, then constantly expressed until 4 h. In addition, total RVV and purified PLA2 caused the release of the eicosanoids; PGE2, TXB2, and LTB4, which reached the peak after 2 h. The findings of this study indicate that purified PLA2 has the potential effects to induce the local inflammation relating the amounts of leukocytes cells, lipid mediators and COX-2 more than the total RVV.

Two resident macrophage subsets reside in peritoneal fluid. Macrophages also reside within mesothelial membranes lining the peritoneal cavity, but they remain poorly characterized. Here, we identified two macrophage populations (LYVE1hi MHC IIlo-hi CX3CR1gfplo/− and LYVE1lo/− MHC IIhi CX3CR1gfphi subsets) in the mesenteric and parietal mesothelial linings of the peritoneum. These macrophages resembled LYVE1+ macrophages within surface membranes of numerous organs. Fate-mapping approaches and analysis of newborn mice showed that LYVE1hi macrophages predominantly originated from embryonic-derived progenitors and were controlled by CSF1 made by Wt1+ stromal cells. Their gene expression profile closely overlapped with ovarian tumor-associated macrophages previously described in the omentum. Indeed, syngeneic epithelial ovarian tumor growth was strongly reduced following in vivo ablation of LYVE1hi macrophages, including in mice that received omentectomy to dissociate the role from omental macrophages. These data reveal that the peritoneal compartment contains at least four resident macrophage populations and that LYVE1hi mesothelial macrophages drive tumor growth independently of the omentum.

Background Primary cystic neoplasms of the peritoneum are rare lesions and not commonly encountered in practice. Many intra-abdominal processes may mimic cystic masses within the peritoneal cavity and pose a diagnostic challenge to both the pathologist and radiologist. Clinical presentation is diverse and varied. These lesions are usually benign. Hence complete surgical excision is the treatment of choice in most of the cases. Methods Study design: Descriptive Retrospective study. Cystic peritoneal lesions were identified and studied from data over a period of 5 years in the Histopathology Section at a tertiary care hospital in Pune, India. Mode of presentation, imaging findings in addition to gross and histopathologic findings of these lesions were studied. Results Out of 50 peritoneal lesions studied over a period of 5 years, only 7 were identified to be cystic peritoneal masses. Of these two were found to be peritoneal cysts, two mesenteric cysts, one an infected mesenteric cyst and one each a mucinous cystadenoma and lymphangioma. Conclusions Correct diagnosis rests in the hands of the pathologist and ensures that the patient receives appropriate and timely management. Hence knowledge of the spectrum of these rare cystic peritoneal masses is necessary to distinguish from other potential cystic abdominal mimicker masses and avoid a potential pitfall.

Gastrointestinal cancer peritoneal metastasis(GICPM) is one of the biggest challenges of clinical treatment. The ultimate solution to the problem requires the clinicians to accurately understand cytologic and molecular pathological mechanisms behind GICPM, and apply such knowledge in the clinical decision-making process for diagnosis and treatment of individual patient, so as to realize "prevention" and "treatment" proactively. The core cytopathological mechanisms behind GICPM, which are closely related to clinical treatment decisions, are as follows: (1) free cancer cells or clusters in peritoneal cavity colonize the peritoneum, resulting in irreversible pathological damage to peritoneal mesothelial cells; (2) the colonized cancer cells further invade the specific structure of the peritoneal milky spots and initiate an accelerated invasive growth process; (3) the process of peritoneal interstitial fibrosis aggravates the structural destruction of the peritoneum; (4) the interaction between cancer cells and immune cells in the milk spots forms a permissive immune microenvironment that promotes the growth of peritoneal metastatic cancer. These four core cytopathological mechanisms are mutually causal and promote each other, forming a vicious circle of GICPM development. As long as clinicians accurately understand these four points, it is possible to grasp the opportunity of clinical diagnosis and treatment, change reactive and passive treatment into preventive and proactive treatment, and improve the clinical diagnosis and treatment landscape of GICPM.胃肠道癌腹膜转移是目前临床治疗的最大难题，解决该难题的根本之道在于临床医生准确把握胃肠道癌腹膜转移的核心细胞病理学机制，基本掌握分子病理学机制，并融会贯通地运用到每一例患者诊治的临床决策过程中，做到"防""治"并举，积极预防、主动治疗。与临床治疗决策密切相关的胃肠道癌腹膜转移的核心细胞病理学机制有4点：（1）腹腔游离癌细胞或微癌灶定植于腹膜，对腹膜间皮细胞造成不可逆病理性损害；（2）定植的癌细胞进一步侵袭腹膜特定结构乳斑，启动加速侵袭性生长过程；（3）腹膜间质纤维化过程加重腹膜的结构性破坏；（4）癌细胞与乳斑中免疫细胞的相互作用，形成促进腹膜转移癌生长的容受性免疫微环境。这4条核心细胞病理学机制互为因果，相互促进，构成腹膜转移发展的恶性循环。临床医生只要准确把握这4点，就有可能掌握临床诊治决策先机，将应对性被动治疗变为预防性主动治疗，改善胃肠道癌腹膜转移临床诊治现状。.

The peritoneal cavity, a fluid-containing potential space surrounding the abdominal and pelvic organs, is home to a rich network of immune cells that maintain tissue homeostasis and provide protection against infection. However, under pathological conditions such as peritonitis, endometriosis, and peritoneal carcinomatosis, the peritoneal immune system can become dysregulated, resulting in nonresolving inflammation and disease progression. An enhanced understanding of the factors that regulate peritoneal immune cells under both homeostatic conditions and in disease contexts is therefore required to identify new treatment strategies for these often life-limiting peritoneal pathologies. Type I interferons (T1IFNs) are a family of cytokines with broad immunoregulatory functions, which provide defense against viruses, bacteria, and cancer. There have been numerous reports of immunoregulation by T1IFNs within the peritoneal cavity, which can contribute to both the resolution or propagation of peritoneal disease states, depending on the specifics of the disease setting and local environment. In this review, we provide an overview of the major immune cell populations that reside in the peritoneal cavity (or infiltrate it under inflammatory conditions) and highlight their contribution to the initiation, progression, or resolution of peritoneal diseases. Additionally, we will discuss the role of T1IFNs in the regulation of peritoneal immune cells, and summarize the results of laboratory studies and clinical trials which have investigated T1IFNs in peritonitis/sepsis, endometriosis, and peritoneal carcinomatosis.

Background and purpose Limited evidence suggests that the sphingosine-1-phosphate/sphingosine kinase 1 (S1P/SPHK1) signaling pathway is involved in the pathogenesis of endometriosis. Therefore, we analyzed in this study whether the inhibition of SPHK1 and, consequently, the reduction of S1P affects the vascularization and growth of endometriotic lesions. Experimental approach Endometriotic lesions were surgically induced in the peritoneal cavity and the dorsal skinfold chamber of female BALB/c mice. The animals received a daily dose of the SPHK1 inhibitor SKI-5C or vehicle (control). Analyses involved the determination of lesion growth, cyst formation, microvessel density and cell proliferation within peritoneal endometriotic lesions by means of high-resolution ultrasound imaging, caliper measurement, histology and immunohistochemistry. In the dorsal skinfold chamber model the development of newly formed microvascular networks and their microhemodynamic parameters within endometriotic lesions were investigated by means of intravital fluorescence microscopy. Key results SKI-5C significantly inhibited the development and vascularization of peritoneal endometriotic lesions, as indicated by a reduced growth and cyst formation, a lower microvessel density and a suppressed cell proliferation when compared to vehicle-treated controls. Endometriotic lesions in dorsal skinfold chambers of SKI-5C-treated animals exhibited a significantly smaller lesion size, lower functional microvessel density, smaller microvessel diameters and a reduced blood perfusion of the newly developing microvascular networks. Conclusions and implications SPHK1/S1P signaling promotes the establishment and progression of endometriotic lesions. The inhibition of this pathway suppresses the development of endometriotic lesions, suggesting SPHK1 as a potential novel target for future endometriosis therapy.

Diffuse alveolar hemorrhage (DAH), although rare, is a life-threatening complication of systemic lupus erythematosus (SLE). Little is known about the pathophysiology of DAH in humans, although increasingly neutrophils, NETosis and inflammatory monocytes have been shown to play an important role in the pristane-induced model of SLE which develops lung hemorrhage and recapitulates many of the pathologic features of human DAH. Using this experimental model, we asked whether endoplasmic reticulum (ER) stress played a role in driving the pathology of pulmonary hemorrhage and what role infiltrating neutrophils had in this process. Analysis of lung tissue from pristane-treated mice showed genes associated with ER stress and NETosis were increased in a time-dependent manner and reflected the timing of CD11b+Ly6G+ neutrophil accumulation in the lung. Using precision cut lung slices from untreated mice we observed that neutrophils isolated from the peritoneal cavity of pristane-treated mice could directly induce the expression of genes associated with ER stress, namely Chop and Bip. Mice which had myeloid-specific deletion of PAD4 were generated and treated with pristane to assess the involvement of PAD4 and PAD4-dependent NET formation in pristane-induced lung inflammation. Specific deletion of PAD4 in myeloid cells resulted in decreased expression of ER stress genes in the pristane model, with accompanying reduction in IFN-driven genes and pathology. Lastly, coculture experiments of human neutrophils and human lung epithelial cell line (BEAS-2b) showed neutrophils from SLE patients induced significantly more ER stress and interferon-stimulated genes in epithelial cells compared to healthy control neutrophils. These results support a pathogenic role of neutrophils and NETs in lung injury during pristane-induced DAH through the induction of ER stress response and suggest that overactivation of neutrophils in SLE and NETosis may underlie development of DAH.

Tissue-engineered vascular grafts (TEVGs) require strategies to allow graft remodeling but avoid stenosis and loss of graft mechanics. A variety of promising biomaterials and methods to incorporate cells have been tested, but intimal hyperplasia and graft thrombosis are still concerning when grafting in small-diameter arteries. Here, we describe a strategy using the peritoneal cavity as an "in vivo" bioreactor to recruit autologous cells to electrospun conduits, which can improve the in vivo response after aortic grafting. We focus on the methods for a novel hydrogel pouch design to enclose the electrospun conduits that can avoid peritoneal adhesion but still allow infiltration of peritoneal fluid and cells needed to provide benefits when subsequently grafting in the aorta.

Introduction: Peritoneal metastases occur in cancers that spread to the peritoneal cavity and indicate the advanced stage of the disease. In children they are mainly seen in sarcomas, Gastrointestinal Stromal Tumors and primary disseminated ovarian tumors. Inflammatory Myofibroblastic Tumor (IMT) is a very rare lesion, characterized by an unpredictable clinical course. The absorption of chemotherapeutic agents through the peritoneal-plasma barrier (PPB) is minimized, thus HIPEC procedure limits the systemic exposure to chemotherapy and permits the administration of its higher doses. The main purpose of HIPEC is to remove the visible macroscopic disease in order to achieve complete cytoreduction (CRS).HIPEC Procedure in Children: Several papers deal with the CRS and HIPEC in children and adolescents, however pediatric experience is still limited. Thus far, the HIPEC procedure has been carried out on patients over 2 years old. The most common indication for the surgery and the best outcome was experienced by patients with desmoplastic small round cell tumor (DSRCT). Most patients received intraperitoneal cisplatin.HIPEC Modification: A 5-month-old infant was admitted to the Department of Pediatric Oncology due to the abdominal distention and blood in the stool. The Computed Tomography (CT) revealed a solid-cystic mass in the right abdominal area. The primary tumor and numerous peritoneal metastasis were removed and the Inflammatory Myofibroblastic Tumor (IMT) was diagnosed. The patient underwent subsequently CRS and modified HIPEC procedure. To avoid overheating of the infant, the intraperitoneal normothermic chemoperfusion was performed. Due to the low body weight a modified dosage of intraperitoneal doxorubicin was used. The child underwent standard postoperative chemotherapy and received crizotinib therapy. At 12 months follow-up since treatment completion the patient remains in complete remission. To our knowledge this is the youngest patient, the only infant and the first pediatric patient with IMT who underwent the modified HIPEC procedure in the world.Conclusions: CRS and HIPEC is technically possible also in infants. For its safe course patients selection and technique modification are necessary. Use of HIPEC should be also considered in intraperitoneally disseminated IMT. A complete cytoreductive surgery as the first HIPEC step seems to be the key factor in survival.