Suppressor Resident Peritoneal Macrophages and Peritonitis Incidence in Continuous Ambulatory Peritoneal Dialysis
| Autor: | Silvano Lamperi, Silvia Carozzi |
|---|---|
| Rok vydání: | 1986 |
| Předmět: |
Adult
Male Bacterial killing Peritonitis In Vitro Techniques Lymphocyte Activation T-Lymphocytes Regulatory Dinoprostone Peritoneal Dialysis Continuous Ambulatory Phagocytosis Reference Values Staphylococcus epidermidis Humans Medicine Prostaglandin E2 Uremia business.industry Macrophages Prostaglandins E Incidence (epidemiology) Continuous ambulatory peritoneal dialysis Interleukin Middle Aged medicine.disease Lymphocyte transformation Immunology Female business Interleukin-1 medicine.drug |
| Zdroj: | Nephron. 44:219-225 |
| ISSN: | 2235-3186 1660-8151 |
| DOI: | 10.1159/000183990 |
| Popis: | Our study was designed to see if peritoneal macrophages (PM) of continuous ambulatory peritoneal dialysis (CAPD) uremic patients, by weakening local defense, could contribute to an increase of peritonitis incidence. Coincubation of nonadherent control responding cells (NACRC) and PM from normal subjects or CAPD patients with low peritonitis incidence (LPI) did not modify blastogenic response of cells to PHA. Coincubation of NACRC and PM from CAPD patients with high peritonitis incidence (HPI) produced noticeable decrease in blastogenic response; these PM, unable to produce normal amounts of Interleukin-1 (IL-1), released large amounts of prostaglandin E2 (PGE2). CAPD patients with LPI and normal subjects produced both substances in similar amounts. PM of CAPD patients with HPI were less able to kill bacteria than those from normal subjects and CAPD patients with LPI, showing a stronger suppressor effect on local defense. This suppressor activity correlated directly to PGE2 release and inversely to IL-1 production. We can hypothesize that in some uremic patients, subpopulations of macrophages growing in response to local stimuli produce humoral substances, negatively affecting cellular-mediated defense and favoring elevated bacterial expansion in peritoneum. |
| Databáze: | OpenAIRE |
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