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Query: UMLS:C0341503 (bacterial peritonitis)
1,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sclerosing peritonitis is a severe complication after CAPD treatment. The visceral peritoneum is thickened and interenteric adhesive parts are found. Myofibroblasts are proliferated and the collageneous tissue is hyperplastic. The mean clinical symptom is the mechanical obstruction of the small bowel. We observed this illness in three out of sixty patients under CAPD. These patients had higher incidence of bacterial peritonitis. In the ascites high concentrations of PG E2 and Thromboxan B2 were observed. After treatment of the infection the concentrations fell down to normal values. Electronoptical observations from peritoneal biopsies showed a proliferation of myofibroblasts and extracellular lysosomes. It is known from these lysosomes that they are able to set free proteasis. These lead to degredation of fibrin and fibrinogen. These splits are mitogen to myofibroblasts. release from HIT cells could also be evoked by the sulphonylureas glibenclamide and tolbutamide and by an increase in concentration of extracellular K+ to 40 mmol/l. The content of cyclic AMP in HIT cells was increased modestly by glucose but not by an increase in extracellular K+. Forskolin elicited a 4-fold increase in cyclic AMP content. We conclude that HIT cells retain the essential features of the insulin secretory response of normal B cells and represent an important tool for further biochemical characterisation of the secretory system.
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PMID:[Sclerosing peritonitis following continuous ambulatory peritoneal dialysis]. 346 44

Bacterial infection triggers host inflammation through the activation of immune cells, leading to the elimination of bacteria. However, the regulatory mechanisms of the host inflammatory response remain unknown. Here we report that a subset of potent tolerogenic dendritic cells (DCs), regulatory DCs (DC(regs)), control the systemic inflammatory response. Unlike normal DCs, which produced proinflammatory cytokines in response to bacterial lipopolysaccharide (LPS), DC(regs) produced fewer proinflammatory cytokines and instead preferentially produced interleukin-10 (IL-10), and these events involved the expression of IkappaBNS and Bcl-3 as well as cyclic AMP (cAMP)-mediated activation of protein kinase A (PKA). In addition, DC(regs) not only suppressed LPS-induced production of proinflammatory cytokines in macrophages, but also reduced their serum levels in mice. Furthermore, DC(regs) protected mice against the lethality induced by experimental endotoxemia and bacterial peritonitis. The inhibitory effect of DC(regs) against inflammatory responses involved the production of IL-10. On the other hand, naturally existing tolerogenic DC subsets producing IL-10, CD11c(low)CD45RB(high) DCs, also suppressed LPS-induced host inflammatory responses. Thus, a subset of tolerogenic DCs act as potential regulators of the host inflammatory response, and they might have preventive and therapeutic potential for the treatment of systemic as well as local inflammatory diseases.
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PMID:Regulatory dendritic cells act as regulators of acute lethal systemic inflammatory response. 1641 Apr 44