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)

We previously described a long-lasting overproduction of nitric oxide (NO) in cirrhotic patients with spontaneous bacterial peritonitis. The aim of the present study was to investigate the presence of the inducible NO pathway in peritoneal macrophages. Ascitic fluids were collected from 29 patients with cirrhosis, aged between 35 and 82 years. Peritoneal macrophages were isolated and cultured in the presence or absence of 1 microg/ml lipopolysaccharide and/or 500 units/ml interferon-gamma (IFN-gamma) for 6 days. NO production was measured as nitrate+nitrite (NO(x)), inducible NO synthase (iNOS) protein expression was analysed by immunocytochemistry and Western blot analysis using a specific anti-(human iNOS) antibody, and the catalytic activity of NOS was revealed by cytochemical staining for NADPH-dependent diaphorase. Cultured macrophages spontaneously released small amounts of NO(x) [median (10-90th percentile) of 18 separate experiments: 3.3 (0-8) micromol/l]. Addition of lipopolysaccharide alone or in combination with IFN-gamma to the culture medium did not change the levels of NO(x), while IFN-gamma alone dramatically increased NO production [13.4 (3.5-28.3) micromol/l; P<0.001]. Macrophages were stimulated by IFN-gamma to a greater extent in patients with recent spontaneous bacterial peritonitis (n=13) than in those in a stable clinical condition (n=18) [19.8 (10.5-30.1) and 10.0 (3.2-14.5) micromol/l respectively; P<0.001]. Macrophages freshly isolated or stimulated with IFN-gamma expressed iNOS protein, as shown by Western blot and immunocytochemical analysis, and stained for NADPH diaphorase. Our findings demonstrate the presence of iNOS protein in peritoneal macrophages from cirrhotic patients. The role of IFN-gamma appears to be a determinant for the up-regulation of NO production, particularly under conditions of infection. Therefore peritoneal macrophages producing large amounts of NO at the site of infection may contribute to maintaining splanchnic vasodilation in these patients.
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PMID:Up-regulation of nitric oxide production by interferon-gamma in cultured peritoneal macrophages from patients with cirrhosis. 1049 39

Suppression of cellular immunity secondary to decreased immunocyte function is one of the surgical stress-induced biological responses. Monocytes/macrophages, natural killer (NK) cells, lymphocytes, and neutrophils play an important role in this immune system. These immunity charge cells are expressed through various surface antigens, such as major histocompatibility complex (MHC) class antigens, T cell receptors, and the cytokines interferon-gamma, interleukin (IL)-2, and IL-12. MHC class II antigen expression of monocytes and the cytokine production of CD4+ T cells are decreased after surgical stress. In this immune-suppressed condition, patients after surgical stress can easily experience infectious complications, and therefore the up-regulation of the immune system is necessary to avoid those complications. Recently, the role of natural immunity as a defense system against infection has received attention. The discovery of Toll-like receptor families revealed how the macrophage system cells recognize microorganisms. Furthermore, liver natural killer(NK) cells and NK T cells are important to induce the Th1 immune response in bacterial peritonitis. In this manuscript, we explain the mechanism of immune suppression after surgical stress and the host defense against infection by analyzing cytokine production and surface membrane molecules in mononuclear cells.
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PMID:[Mechanism of immune suppression after surgical stress and host defense against infection]. 1473 64