Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031154 (peritonitis)
 15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies on human macrophages are restricted due to difficulties in isolating significant numbers of human macrophages. High numbers of monocytes/macrophages can be obtained from peritonitis effluents of patients treated with peritoneal dialysis. To determine whether these cells might be useful for functional studies, we characterized peritoneal macrophages (PM) immediately after isolation from the dialysate effluents and their subsequent differentiation. During a 10 days culture period they differentiated morphologically and phenotypically (FACS-analysis) from monocyte-like cells to macrophages. Reflecting the intraperitoneal inflammation we found protein- and mRNA-synthesis of IL-8 and monocyte-chemoattractant-protein-1 (MCP-1) to be upregulated in PM after isolation from the effluents. In contrast, TNF-alpha was downregulated and could not be stimulated by LPS and/or IFN-gamma, reflecting the phenomenon of desensitization. After 10 days in culture, cytokine production normalized to a constitutive level and the TNF-alpha responsiveness to LPS was restored. These data suggest the recovery of PM from the inflammatory prestimulation. Therefore PM harvested from peritoneal dialysis effluents might provide a useful tool for further studies on the role of human macrophages in inflammation.
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PMID:In vitro differentiation and characterization of human peritoneal macrophages from CAPD-peritonitis patients. 1008 96

Polymorphonuclear leukocytes (PMN) release gelatinase B in response to variable stimuli. Gelatinase B degrades basement membrane components in vitro, and inhibition of matrix metalloproteinase activity blunts PMN migration through a prototype basement membrane (Matrigel) and amnionic membranes. Accordingly, it has been speculated that gelatinase B is necessary for PMN emigration. To test this hypothesis we induced acute inflammation in the lungs, peritoneum, and skin in mice with a null mutation of the gelatinase B gene (gelatinase B-/-) and littermate controls (gelatinase B+/+). At 3, 6, 12, and 24 h after intratracheal instillation of LPS, the emigration of PMN in the lung, as determined by PMN in bronchoalveolar lavage fluid, was similar in gelatinase B-/- and gelatinase B+/+ mice. The number of PMN in the peritoneal cavity 4 h after thioglycollate-induced peritonitis was also comparable in gelatinase B-/- and gelatinase B+/+ mice. At 4 h after an intradermal injection of interleukin-8, numerous PMN were present extravascularly in the dermis in both gelatinase B-/- and gelatinase B+/+ mice and the myeloperoxidase activities of the skin at the injection sites were indistinguishable between the two types of mice. PMN from gelatinase B-/- mice migrated through Matrigel in response to zymosan-activated serum with the same efficiency as did PMN from gelatinase B+/+ mice. In vitro, gelatinase B-/- PMN killed Staphylococcus aureus and Klebsiella pneumoniae as effectively as did PMN from gelatinase B+/+ mice. These findings indicate that gelatinase B is not required for PMN emigration, and suggest that the antibacterial function of PMN is preserved despite gelatinase B deficiency.
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PMID:Neutrophil emigration in the lungs, peritoneum, and skin does not require gelatinase B. 1034 Sep 50

The murine CC chemokine C10, a macrophage chemoattractant, has been shown to have an unusually restricted expression pattern in cultured cells (LPS non-responsive, IL-4 inducible). Its occurrence in vivo has not been characterized. Here the authors employ immunocytochemistry to demonstrate that C10 is expressed in inflammatory macrophages during irritant peritonitis. In addition, C10 was found to be a constitutive component of eosinophils. Peritoneal inflammation led to the accumulation of sufficient C10 (> 10 nM) to permit detection in exudate fluid. This accumulation did not begin until 24h after challenge, and was sustained through at least day 10 of the inflammation. In contrast, MIP-1alpha gene expression was earlier and transient. These kinetic features are consistent with earlier in vitro findings, suggesting that C10 is not a "first-wave" chemokine and may play a role related to chronic stages of host defence reactions.
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PMID:Sustained high-level production of murine chemokine C10 during chronic inflammation. 1041 54

Peritonitis induced by cecal ligation and puncture (CLP) produces a systemic inflammatory response that can be largely mitigated by pretreatment of the animals with lipopolysaccharide (LPS tolerance). Although cells of myeloid origin and endothelial cells have been shown to contribute to the development of LPS tolerance, little is known regarding the potential role of parenchymal cells in this phenomenon. The major aim of the present study was to assess whether cardiac parenchymal cells (myocytes) contribute to the development of LPS tolerance. Six hours after induction of CLP rats were neutropenic and acidotic, the myocardium contained a leukocyte infiltrate [myeloperoxidase (MPO) activity was increased], and myocardial contractile function was impaired (left ventricular developed pressure was decreased). In animals that were pretreated with LPS these manifestations of sepsis were largely reversed. Further studies focused on the responses of cardiac myocytes to CLP and whether myocytes contributed to the development of LPS tolerance. Myocytes were isolated from rat hearts 6 h after induction of CLP. These myocytes 1) exhibited an impaired ability to shorten in response to pacing, 2) contained the nuclear transcription factor NF-kappaB in their nuclei, 3) increased their surface levels of intercellular adhesion molecule-1 (ICAM-1), and 4) were hyperadhesive for neutrophils. All of these events did not occur in myocytes obtained from animals that were pretreated with LPS before induction of CLP. These findings indicate that LPS tolerance can be induced in myocytes with respect to polymorphonuclear leukocyte adhesion, presumably by an inability of CLP to mobilize NF-kappaB to the myocyte nuclei and, thereby, preventing an increase in surface levels of ICAM-1.
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PMID:LPS pretreatment ameliorates peritonitis-induced myocardial inflammation and dysfunction: role of myocytes. 1048 7

Fever, a nonspecific acute-phase response, has been associated with improved survival and shortened disease duration in infections, but the mechanisms of these beneficial responses are poorly understood. We previously reported that increasing core temperature of bacterial endotoxin (LPS)-challenged mice to the normal febrile range modified expression of tumor necrosis factor alpha (TNF-alpha), interleukin 1beta (IL-1beta), and IL-6, three cytokines critical to mounting an initial defense against microbial pathogens, but survival was not improved in the warmer animals. We speculated that our inability to show a survival benefit of optimized cytokine expression in the warmer animals reflected our use of LPS, a nonreplicating agonist, rather than an infection with viable pathogens. The objective of this study was to determine if increasing murine core temperature altered cytokine expression and improved survival in an experimental bacterial peritonitis model. We showed that housing mice at 35.5 degrees C rather than 23 degrees C increased core temperature from 36.5 to 37.5 degrees C to 39.2 to 39.7 degrees C, suppressed plasma TNF-alpha expression for the initial 48 h, delayed gamma interferon expression, improved survival, and reduced the bacterial load in mice infected with Klebsiella pneumoniae peritonitis. We showed that the reduced bacterial load was not caused by a direct effect on bacterial proliferation and probably reflected enhanced host defense. These data suggest that the increase in core temperature that occurs during bacterial infections is essential for optimal antimicrobial host defense.
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PMID:Febrile core temperature is essential for optimal host defense in bacterial peritonitis. 1067 36

The innate immune system provides essential information about the presence of infectious danger and signals the activation and instruction of adaptive immunity. The present study addressed the question of whether prior exposure of the innate immune system to LPS may modulate host defense against acute septic peritonitis. We show that LPS priming 4 days, but not 2 days, prior to infection enhances bacterial clearance and improves survival of septic peritonitis. Immune protection in day 4 LPS-primed mice was specifically associated with a marked increase in the accumulation and activation of neutrophils at the site of infection. Accumulating neutrophils in day 4 LPS-primed mice exhibited a normal production of reactive oxygen metabolites in response to in vivo exposure to intestinal bacteria. The local increase in neutrophil numbers was found to result from a reduced rate of apoptotic cell death. Inhibition of neutrophil apoptosis in LPS-primed mice was mediated by soluble factor(s) distinct from G-CSF and GM-CSF. Thus, engagement of pattern recognition systems prior to infection may improve host defense by amplifying the effector cell response of innate immunity. The results also provide in vivo evidence that apoptosis of inflammatory cells represents an important process for the control of host defense to infection.
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PMID:Immune protection against septic peritonitis in endotoxin-primed mice is related to reduced neutrophil apoptosis. 1129 54

Toll-like receptors (TLRs) are mammalian homologues of the Drosophila Toll receptors and are thought to have roles in innate recognition of bacteria. We demonstrated that TLR 2, 4, 6, and 8 but not TLR5 were expressed on mouse bone marrow-derived mast cells (BMMCs). Using BMMCs from the genetically TLR4-mutated strain C3H/HeJ, we demonstrated that functional TLR4 was required for a full responsiveness of BMMCs to produce inflammatory cytokines (IL-1beta, TNF-alpha, IL-6, and IL-13) by LPS stimulation. TLR4-mediated stimulation of mast cells by LPS was followed by activation of NF-kappaB but not by stress-activated protein kinase/c-Jun NH2-terminal kinase signaling. In addition, in the cecal ligation and puncture-induced acute septic peritonitis model, we demonstrated that genetically mast cell-deficient W/W(v) mice that were reconstituted with TLR4-mutated BMMCs had significantly higher mortality than W/W(v) mice reconstituted with TLR4-intact BMMCs. Higher mortality of TLR4-mutated BMMC-reconstituted W/W(v) mice was well correlated with defective neutrophil recruitment and production of proinflammatory cytokines in the peritoneal cavity. Taken together, these observations provide definitive evidence that mast cells play important roles in exerting the innate immunity by releasing inflammatory cytokines and recruitment of neutrophils after recognition of enterobacteria through TLR4 on mast cells.
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PMID:Protective roles of mast cells against enterobacterial infection are mediated by Toll-like receptor 4. 1149 12

Polymorphonuclear leukocytes (PMN) and LPS-binding protein (LBP) are both components of the innate immune system. LBP is a plasma protein that binds to lipid A and enhances the biological activity of LPS 100- to 1000-fold. Recently it was reported that LBP-deficient mice are more susceptible to Salmonella typhimurium infection. Here we report that LBP KO mice are more susceptible to Salmonella peritonitis, but not to oral or i.v. infection. LBP knockout (KO) mice responded normally to i.p. injections of Staphylococcus aureus and casein, but not to i.p. injection of S. typhimurium or Salmonella LPS. Mice with a mutation in Toll-like receptor 4 (C3H/HeJ) have a similar defect in PMN chemotaxis. In normal mice S. typhimurium stimulated production of the CXC chemokines macrophage inflammatory protein-2 and cytokine-induced neutrophil chemoattractant, but levels of cytokine-induced neutrophil chemoattractant and macrophage inflammatory protein-2 were greatly reduced in the LBP KO mice. LBP KO mice pretreated with casein to attract PMN in an LBP-independent manner were more resistant to Salmonella infection, but neutropenic mice were not protected by casein. Splenic TNF-alpha mRNA levels were also lower in LBP KO than in control mice infected with Salmonella. Since TNF-alpha can activate PMN, LBP KO mice may have both fewer and less active PMN in the first few hours after Salmonella are injected, making LBP KO mice more susceptible. This work confirms the importance of PMN in resistance to Salmonella infections and shows that this is facilitated by LBP.
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PMID:The role of lipopolysaccharide binding protein in resistance to Salmonella infections in mice. 1205 58

Pretreatment of mice with low quantities of LPS induces endotoxin tolerance characterized by enhanced resistance to lethal doses of LPS and to a number of infectious challenges. Mice subjected to cecal ligation and puncture (CLP) survived the ensuing septic peritonitis significantly better when they had been pretreated with LPS. This LPS-induced protection was dependent on endogenous TNF production capacity since LPS pretreatment did not protect TNF-deficient mice from death after CLP. While mice deficient in the TNF receptor type 2 (p75TNFR) were as sensitive to CLP-induced mortality as control mice, LPS pretreatment could not reduce mortality in p75TNFR-deficient mice after CLP. Therefore, activation of the TNF receptor type 2 by endogenous TNF constitutes an important interaction for the development of LPS-induced resistance to bacterial infection.
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PMID:Requirement of TNF and TNF receptor type 2 for LPS-induced protection from lethal septic peritonitis. 1253 95

MATISSE is a new endotoxin (ET) adsorption system. It comprises the FRESENIUS hemoadsorption machine 4008 ADS to maintain the extracorporeal circuits and disposables including the MATISSE-adsorber based on macroporous beads immobilized with human serum albumin. In vivo and in vitro experiments with this new compound had shown favourable ET elimination properties. In a first study 19 healthy volunteers were included for the safety and tolerability of the endotoxin adsorber system. One single veno-venous hemoperfusion with this system was performed. Apheresis treatment with the human albumin immobilized adsorber seems to be safe and well tolerable in healthy volunteers. A slight decrease in platelet count as well as insulin level was observed. No serious adverse events were mentioned. Similar findings were made in an open uncontrolled trial in six patients with suspected Gram-negative sepsis. Here endotoxin adsorption seems to be safe and well tolerated without adsorber related major adverse events. In the last clinical trial including 145 patients mainly peritonitis patients (104), again no safety concerns were found during the apheresis. Trends in improvement of morbidity and organ dysfunction were found as well as efficient LPS removal in peritonitis patients. LPS whole blood immunoadsorption is a promising new method. No relevant side effects were observed so far. A large controlled study to prove clinical efficacy in patients with severe sepsis and confirmed endotoxemia (e.g. peritonitis) should be necessary.
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PMID:A new endotoxin adsorption device in Gram-negative sepsis: use of immobilized albumin with the MATISSE adsorber. 1287 99


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