Peritoneal Defenses Against Infection: Winning the Battle but Losing the War?

Faull, Randall J.

doi:10.1046/j.1525-139x.2000.00013.x

Cited by 15 publications

(16 citation statements)

References 82 publications

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“…Another important function of the peritoneal mesothelium in the setting of chronic PD is defence against peritonitis [4]. Under normal circumstances the mesothelial lining acts as a physical barrier to microbial invasion, but this is compromised in patients on PD as a result of the artificial conditions imposed by the instillation of hypertonic glucose solutions.…”

Section: Introductionmentioning

confidence: 99%

Regulation of complement C3 and C4 synthesis in human peritoneal mesothelial cells by peritoneal dialysis fluid

Tang

Leung

Chan

et al. 2004

Clinical and Experimental Immunology

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SUMMARYAlthough complement is activated in the peritoneal cavity during chronic peritoneal dialysis (PD), little is known about its role in peritoneal defence and injury related to long-term PD. We examined the impact of glucose and commercial peritoneal dialysis solutions on complement expression in HPMCs obtained by primary culture from omental tissues of consented patients undergoing elective abdominal surgery. Constitutive expression of C3 and C4 mRNA in HPMCs was up-regulated upon exposure to 75 m M glucose in a time-dependent manner. C3 and C4 protein was secreted in both apical and basolateral directions. Glucose doses beyond 100 m M markedly down-regulated C3 and C4 expression, and stimulated LDH release dose-dependently. Such cytotoxic effects were attenuated using equivalent doses of mannitol instead of glucose. Treatment with conventional lactate-buffered dialysis solution gave rise to down-regulation of C3 and C4 expression, and heightened LDH release in HPMCs. These effects correlated with the glucose strength of the solution, persisted despite replacement with a bicarbonate-buffered solution, aggravated by glycated albumin, and were partially abrogated by supplementation with 10% fetal bovine serum in the culture system. Our findings suggest that the artificial conditions imposed by PD lead to alterations in local complement synthesis that have implications for the role of the peritoneal mesothelium in both inflammation and defence.

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Section: Introductionmentioning

confidence: 99%

Regulation of complement C3 and C4 synthesis in human peritoneal mesothelial cells by peritoneal dialysis fluid

Tang

Leung

Chan

et al. 2004

Clinical and Experimental Immunology

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“…At this inflammatory stage, the main signals that activate PMC are probably proinflammatory cytokines such as IL-1 and TNF-a secreted from resident peritoneal macrophages. These cytokines induce PMC to mainly secrete chemoattractants of granulocytes, such as IL-8 which precipitates the recruitment of neutrophils [25][26][27]. Indeed our data demonstrate that the mRNA of KC, the mouse analogue of IL-8, is strongly induced in PMC at first hours of inflammation.…”

Section: Discussionmentioning

confidence: 67%

CD40 ligand (CD154) takes part in regulation of the transition to mononuclear cell dominance during peritonitis

Mazar

Agur

Rogachev

et al. 2005

Kidney International

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“…This will be compounded by the nature of the underlying event. Within the abdomen, activation of coagulation, cytokine and other inflammatory cascades results in a copious fluid and cellular response in the first 48 h 32 but will continue at a slower rate while the abdomen remains open. The systemic inflammatory response 33,34 is likely to be severe, especially if the underlying pathology is severe and ongoing, for example, pancreatitis, or an ongoing peritonitis.…”

Section: The Consequences Of Oamentioning

confidence: 99%

“…The initial process is characterized by fibrin deposition and collagenization. Subsequently, fibrinolysis predominates, 32 and laparotomy may not be possible after this for at least 6 weeks and possibly a lot longer, until this process is complete.…”

Section: The Consequences Of Oamentioning

confidence: 99%