Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0341503 (bacterial peritonitis)
 1,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During bacterial peritonitis of patients on continuous ambulatory peritoneal dialysis (CAPD) leukocytes, particularly polymorphonuclear neutrophilic granulocytes (PMNs), migrate into the peritoneal cavity. However, at the site of inflammation PMNs are not sufficiently able to protect the host against micro-organisms. Adhesion molecules, such as ICAM-1 (CD54), are involved in the interaction between endothelial cells and PMNs leading to the accumulation of PMNs at the site of inflammation. As PMNs are the predominant cell type in the peritoneal cavity in peritonitis, the aim of this study was to find out whether PMNs from CAPD peritonitis patients were able to express ICAM-1. Flow cytometric analyses with the anti-CD54 monoclonal antibody demonstrated that normal PMNs constitutively express slight amounts of ICAM-1. In contrast to normal PMNs, peritoneal PMNs from patients with CAPD peritonitis expressed high amounts of ICAM-1 (p = 0.003). Furthermore, ICAM-1 expression on peripheral blood PMNs of these patients significantly differed from PMNs from healthy donor (p = 0.01). Furthermore, Northern blot analysis revealed a weak signal of ICAM-1 mRNA in normal PMNs. However, peritoneal PMNs from CAPD peritonitis patients expressed a strong signal for ICAM-1 mRNA, suggesting that ICAM-1 is newly synthesized when PMNs invade the peritoneal cavity. In summary, this study clearly demonstrates that peritoneal PMNs of CAPD peritonitis express high amounts of ICAM-1 receptor on the level of mRNA and on the surface. Therefore, it is tempting to speculate that peritoneal PMNs interact amongst each other between ICAM-1 and its counter receptors CD11a,b/CD18 receptor.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Synthesis and surface expression of ICAM-1 in polymorphonuclear neutrophilic leukocytes in normal subjects and during inflammatory disease. 852 60

Bacterial peritonitis is the most important complication of peritoneal dialysis (PD), limiting its widespread application. Conventional glucose-based peritoneal dialysates (G-PDS) depress oxygen consumption, chemiluminescence, superoxide production, phagocytosis, bacterial killing and actin polymerization in neutrophils (PMN) in vitro. Expression of adhesion receptors is critical to leukocyte activation, adhesion, migration and phagocytosis. The effects of G-PDS on basal and stimulated leukocyte adhesion molecule expression and leukocyte adhering capacity is unknown. We examined the effect of a five minutes incubation of whole blood in either HEPES-buffered saline or G-PDS containing 1.5% (83 mM), 2.5% (139 mM) or 4.25% (236 mM) glucose, at pH = 5.2, and pH = 7.4. PMN intracellular pH was measured spectrofluorometrically. Leukocyte CD11b, CD18 and CD14 were measured by flow cytometry using monoclonal antibodies in otherwise unstimulated cells or 60 minutes after lipopolysaccharide (LPS) stimulation. In addition, leukocyte adhering capacity to nylon wool was tested. In an attempt to dissect the effect of high glucose concentrations from that of the attendant hyperosmolality, the experiments were repeated with dialysates in which glucose was substituted by sodium chloride (NaCl-PDS) to attain identical osmolalities. G-PDS, as well as the mixtures of spent and fresh G-PDS, significantly depressed the basal PMN expression of adhesion receptors CD11b and CD18 and monocyte expression of CD14, and substantially mitigated the LPS-mediated up-regulation of CD11b and CD18. Likewise, G-PDS significantly inhibited leukocyte adhering capacity without affecting cell viability. Similar results were observed with NaCl-PDS. The observed abnormalities were primarily osmolality-dependent, and largely intra- and extracellular pH-independent. Impaired adhesion receptor expression and cell adhesion capacity shown here reveal another dimension of the G-PDS-induced leukocyte abnormalities.
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PMID:Effects of conventional peritoneal dialysates on leukocyte adhesion and CD11b, CD18 and CD14 expression. 891 36