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Fel'dsher I Akusherka Apr 1952
Topics: Disease; Peritoneal Diseases; Peritoneum; Peritonitis, Tuberculous; Tuberculosis
PubMed: 14926725
DOI: No ID Found -
Journal of Immunology (Baltimore, Md. :... Jul 2009Fungal peritonitis is an important complication in peritoneal dialysis patients; either continuous or recurrent peritonitis may enhance peritoneal damage. Even when the...
Fungal peritonitis is an important complication in peritoneal dialysis patients; either continuous or recurrent peritonitis may enhance peritoneal damage. Even when the peritoneal dialysis catheter is removed in patients with fungal peritonitis, peritoneal fibrosis can progress and evolve into encapsular peritoneal sclerosis. It is unclear why fungal infections are worse than bacterial in these respects. Zymosan is a cell wall component of yeast that strongly activates the complement system. In this study, we compared the effects of zymosan and bacterial LPS on peritoneal inflammation in a rat peritoneal injury model induced by mechanical scraping. Intraperitoneal administration of zymosan, but not LPS or vehicle, caused markedly enhanced peritonitis with massive infiltration of cells and deposition of complement activation products C3b and membrane attack complex on day 5. In rats administered zymosan and sacrificed on days 18 or 36, peritoneal inflammation persisted with accumulation of ED-1-positive cells, small deposits of C3b and membrane attack complex, exudation of fibrinogen, and capillary proliferation in subperitoneal tissues. When zymosan was administered daily for 5 days after peritoneal scrape, there was even greater peritoneal inflammation with peritoneal thickening, inflammatory cell accumulation, and complement deposition. Inhibition of systemic complement by pretreatment with cobra venom factor or local inhibition by i.p. administration of the recombinant complement regulator Crry-Ig reduced peritoneal inflammation in zymosan-treated rats. Our results show that yeast components augment inflammation in the injured peritoneum by causing complement activation within the peritoneal cavity. Local anticomplement therapy may therefore protect from peritoneal damage during fungal infection of the peritoneum.
Topics: Animals; Cell Movement; Complement Activation; Complement C3b; Complement Membrane Attack Complex; Disease Models, Animal; Lipopolysaccharides; Male; Neovascularization, Pathologic; Peritoneum; Peritonitis; Rats; Rats, Sprague-Dawley; Yeasts; Zymosan
PubMed: 19553534
DOI: 10.4049/jimmunol.0804245 -
Kidney International Aug 2018The effect of peritoneal dialysates with low-glucose degradation products on peritoneal membrane morphology is largely unknown, with functional relevancy predominantly... (Observational Study)
Observational Study
The effect of peritoneal dialysates with low-glucose degradation products on peritoneal membrane morphology is largely unknown, with functional relevancy predominantly derived from experimental studies. To investigate this, we performed automated quantitative histomorphometry and molecular analyses on 256 standardized peritoneal and 172 omental specimens from 56 children with normal renal function, 90 children with end-stage kidney disease at time of catheter insertion, and 82 children undergoing peritoneal dialysis using dialysates with low-glucose degradation products. Follow-up biopsies were obtained from 24 children after a median peritoneal dialysis of 13 months. Prior to dialysis, mild parietal peritoneal inflammation, epithelial-mesenchymal transition and vasculopathy were present. After up to six and 12 months of peritoneal dialysis, blood microvessel density was 110 and 93% higher, endothelial surface area per peritoneal volume 137 and 95% greater, and submesothelial thickness 23 and 58% greater, respectively. Subsequent peritoneal changes were less pronounced. Mesothelial cell coverage was lower and vasculopathy advanced, whereas lymphatic vessel density was unchanged. Morphological changes were accompanied by early fibroblast activation, leukocyte and macrophage infiltration, diffuse podoplanin presence, epithelial mesenchymal transdifferentiation, and by increased proangiogenic and profibrotic cytokine abundance. These transformative changes were confirmed by intraindividual comparisons. Peritoneal microvascular density correlated with peritoneal small-molecular transport function by uni- and multivariate analysis. Thus, in children on peritoneal dialysis neutral pH dialysates containing low-glucose degradation products induce early peritoneal inflammation, fibroblast activation, epithelial-mesenchymal transition and marked angiogenesis, which determines the PD membrane transport function.
Topics: Adolescent; Biopsy; Case-Control Studies; Child; Child, Preschool; Dialysis Solutions; Epithelial-Mesenchymal Transition; Female; Fibrosis; Glucose; Humans; Hydrogen-Ion Concentration; Infant; Kidney Failure, Chronic; Male; Peritoneal Dialysis; Peritoneum; Peritonitis; Treatment Outcome
PubMed: 29776755
DOI: 10.1016/j.kint.2018.02.022 -
Kidney International. Supplement Dec 1994
Review
Topics: Cytokines; Fibroblasts; Humans; Macrophages, Peritoneal; Peritoneal Dialysis, Continuous Ambulatory; Peritoneum; Peritonitis; Prostaglandins
PubMed: 7700045
DOI: No ID Found -
The Journal of Surgical Research Mar 2020Implants used in abdominal wall reconstruction are associated with intra-abdominal inflammation that can cause complications such as adhesions, fistulae, or failure of...
BACKGROUND
Implants used in abdominal wall reconstruction are associated with intra-abdominal inflammation that can cause complications such as adhesions, fistulae, or failure of the implant. This study analyzed the inflammatory response of human peritoneum explants when exposed to different implant materials including synthetic and biological (cross-linked and non-cross-linked).
MATERIALS AND METHODS
Human peritoneum explants (parietal and visceral) were incubated in culture with implants used for abdominal wall reconstruction. Implants included Permacol (biological implant with chemical cross-linking); Biodesign and Strattice (biological implants without chemical cross-linking); Prolene (synthetic nonabsorbable); and Vicryl (synthetic absorbable). Control peritoneum samples were incubated without implant. Cytokine concentrations and corresponding gene expression were measured by enzyme-linked immunosorbent assay and quantitative polymerase chain reaction, respectively. Further evaluation included assessment of tissue viability and implant-cytokine adsorption.
RESULTS
Incubation of human peritoneal explants with Biodesign or Strattice was associated with a significant reduction in interleukin-6, interleukin-1β, and tumour necrosis factor alpha protein and gene expression compared with control. These could not be explained by reduced cell viability or implant-cytokine adsorption. Incubation of explants in Biodesign-conditioned media displayed a similar effect to incubation of explants with Biodesign itself.
CONCLUSIONS
Human peritoneal explants cultured with different mesh implant materials show an altered inflammatory cytokine response suggesting a tissue-specific response. Downregulation of key inflammatory cytokines by the peritoneum exposed to non-cross-linked biological implants may be mediated by the release of soluble factors from these implants inhibiting cytokine gene expression. This ex vivo human peritoneal system provides a novel preclinical model to investigate peritoneum-implant interactions.
Topics: Abdominal Wall; Cytokines; Gene Expression Profiling; Humans; Incisional Hernia; Materials Testing; Peritoneum; Peritonitis; Prostheses and Implants; Plastic Surgery Procedures; Surgical Mesh; Tissue Adhesions; Tissue Culture Techniques
PubMed: 31753555
DOI: 10.1016/j.jss.2019.10.022 -
PloS One 2011Mammals are serially infected with a variety of microorganisms, including bacteria and parasites. Each infection reprograms the immune system's responses to re-exposure...
Mammals are serially infected with a variety of microorganisms, including bacteria and parasites. Each infection reprograms the immune system's responses to re-exposure and potentially alters responses to first-time infection by different microorganisms. To examine whether infection with a metazoan parasite modulates host responses to subsequent bacterial infection, mice were infected with the hookworm-like intestinal nematode Nippostrongylus brasiliensis, followed in 2-4 weeks by peritoneal injection of the pathogenic bacterium Klebsiella pneumoniae. Survival from Klebsiella peritonitis two weeks after parasite infection was better in Nippostrongylus-infected animals than in unparasitized mice, with Nippostrongylus-infected mice having fewer peritoneal bacteria, more neutrophils, and higher levels of protective interleukin 6. The improved survival of Nippostrongylus-infected mice depends on IL-4 because the survival benefit is lost in mice lacking IL-4. Because mast cells protect mice from Klebsiella peritonitis, we examined responses in mast cell-deficient Kit(W-sh)/Kit(W-sh) mice, in which parasitosis failed to improve survival from Klebsiella peritonitis. However, adoptive transfer of cultured mast cells to Kit(W-sh)/Kit(W-sh) mice restored survival benefits of parasitosis. These results show that recent infection with Nippostrongylus brasiliensis protects mice from Klebsiella peritonitis by modulating mast cell contributions to host defense, and suggest more generally that parasitosis can yield survival advantages to a bacterially infected host.
Topics: Animals; Interleukin-6; Intestines; Klebsiella Infections; Klebsiella pneumoniae; Likelihood Functions; Mast Cells; Mice; Neutrophil Infiltration; Nippostrongylus; Peritoneum; Peritonitis; Sepsis; Survival Analysis
PubMed: 22110673
DOI: 10.1371/journal.pone.0027564 -
American Journal of Surgery Oct 2011The aim of this study was to evaluate the peritoneal computed tomography (CT) attenuation values and relate them to the severity of peritonitis in patients with...
BACKGROUND
The aim of this study was to evaluate the peritoneal computed tomography (CT) attenuation values and relate them to the severity of peritonitis in patients with gastrointestinal tract (GI) perforations.
METHODS
A total of 56 consecutive patients with GI perforations who underwent CT scan and emergency laparotomy in our hospital were enrolled in this study. The CT attenuation values of the peritoneum were measured on a workstation by 2 independent investigators, and were investigated in relation to the severity of illness and hospital mortality.
RESULTS
Peritoneal CT attenuation values in hospital nonsurvivors were significantly lower than those in survivors. There was significant negative correlation between peritoneal CT attenuation values and sequential organ failure assessment score, acute physiology and chronic health evaluation II score, and the Mannheim peritonitis index.
CONCLUSIONS
The evaluation of peritoneal CT attenuation values in patients with peritonitis is simple and can be used for objective assessment of the severity of peritonitis.
Topics: Adult; Aged; Aged, 80 and over; Female; Hospital Mortality; Humans; Intestinal Perforation; Male; Middle Aged; Peptic Ulcer Perforation; Peritoneum; Peritonitis; Severity of Illness Index; Stomach Diseases; Tomography, X-Ray Computed
PubMed: 21943948
DOI: 10.1016/j.amjsurg.2010.08.037 -
American Journal of Physiology. Renal... Dec 2013In peritoneal dialysis (PD) therapy, physical stresses such as exposure to peritoneal dialysate, catheter trauma, and peritonitis may induce peritoneal injury that can...
In peritoneal dialysis (PD) therapy, physical stresses such as exposure to peritoneal dialysate, catheter trauma, and peritonitis may induce peritoneal injury that can prevent continued long-term PD therapy. Therefore, protection of the peritoneum is an important target to enable long-term PD therapy in patients with end-stage renal disease. We previously showed that neutralization of the membrane complement regulators (CRegs) Crry and CD59 in rat peritoneum provokes development of acute peritoneal injury due to uncontrolled complement activation. C5a is a key effecter molecule of the complement system released during acute inflammation. Control of C5a has been proposed as a strategy to suppress inflammatory reactions and, because peritoneal injury is accompanied by inflammation, we hypothesized that C5a targeted therapy might be an effective way to suppress peritoneal injury. In the present study we used an established acute peritonitis model induced by neutralization of CRegs to investigate the effects on acute peritoneal injury of inhibiting C5a. Intravenous administration of an anti-C5a complementary peptide (AcPepA) up to 4 h after induction of injury significantly and dose-dependently prevented accumulation of inflammatory cells and reduced tissue damage in the model, accompanied by decreased C3b deposition. We show that C5a contributed to the development of peritoneal injury. Our results suggest that C5a is a target for preventing or treating peritoneal injury in patients undergoing prolonged PD therapy or with infectious complications.
Topics: Animals; Antibodies; Antigens, Protozoan; Antigens, Surface; CD59 Antigens; Complement Activation; Disease Models, Animal; Male; Peptide Fragments; Peritoneal Dialysis; Peritoneum; Peritonitis; Rats; Rats, Sprague-Dawley; Receptors, Cell Surface
PubMed: 23904221
DOI: 10.1152/ajprenal.00681.2012 -
Peritoneal Dialysis International :... Jun 2007During peritoneal dialysis, peritoneal cells are repeatedly exposed to a non-physiologic hypertonic environment with high glucose content and low pH. Current sterile... (Review)
Review
During peritoneal dialysis, peritoneal cells are repeatedly exposed to a non-physiologic hypertonic environment with high glucose content and low pH. Current sterile dialysis solutions cause inflammation in the submesothelial compact zone, leading to fibrosis, angiogenesis, and, eventually, ultrafiltration failure. Although the normal interstitium separates the peritoneal microvasculature from the dialysis fluid and makes transperitoneal transport less efficient, changes in the submesothelial compact zone can result in progressive increases in solute transfer and ultrafiltration diminution. This peritoneal dysfunction will further be amplified with the development of an epithelial-to-mesenchymal transition of mesothelial cells and dissipation of the osmotic driving force through the increased area and solute transport that accompany neoangiogenesis of the submesothelial microvasculature. The alteration of the peritoneal membrane can be further aggravated by peritonitis, advanced glycation end-products, and glucose degradation products. Furthermore, new data are emerging to support a proinflammatory role for peritoneal adipocytes.
Topics: Dialysis Solutions; Epithelium; Fibrosis; Humans; Inflammation; Inflammation Mediators; Kidney Failure, Chronic; Peritoneal Dialysis; Peritoneum; Peritonitis; Ultrafiltration
PubMed: 17556333
DOI: No ID Found -
Contributions To Nephrology 2006Peritoneal sclerosis is very common in peritoneal dialysis (PD) patients. It can vary from the mild, clinically silent sclerosis always present after years of PD, to... (Review)
Review
Peritoneal sclerosis is very common in peritoneal dialysis (PD) patients. It can vary from the mild, clinically silent sclerosis always present after years of PD, to rare but dramatic and often fatal cases. In our opinion, peritoneal sclerosis is a single disorder, so its variable manifestations are different stages of one nosological entity: this opinion relies mainly on strong connections in pathophysiology. In our view, the frequency, pathology, animal models, etiology and pathogenesis often show a bimodal configuration with suggests that peritoneal sclerosis is actually two distinct nosological entities: simple sclerosis and sclerosing peritonitis. The former is very frequent, with minor anatomical alterations and low clinical impact; it is reproducible in animals by means of PD, and is clearly due to the poor biocompatibility of PD. The latter is rare, with radical anatomical alterations and high mortality; it can only be reproduced in animal models by means other than PD and seems to be due to factors both related and unrelated to PD.
Topics: Animals; Fibrosis; Humans; Models, Animal; Peritoneal Dialysis; Peritoneum; Peritonitis; Sclerosis
PubMed: 16720993
DOI: 10.1159/000093503