The macrophage response to bacteria: Flow of L-arginine through the nitric oxide and urea pathways and induction of tumoricidal activity

Keller, R.; Keist, Ruth; Klauser, Stephan; Schweiger, Ana

doi:10.1016/0006-291x(91)91863-8

Cited by 24 publications

(9 citation statements)

References 13 publications

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“…Earlier work showing that secretion of NO and N02 and expression of tumoricidal activity by macrophages were both suppressed by agents that interfere with L-arginine, such as arginase or analogs of L-arginine, and that suppression was reversed by L-arginine provided evidence for the involvement of L-arginine-dependent mechanisms (24,27,29,30,33,35). The present experiments with NMMA led to a similar conclusion ( Table 5).…”

Section: Tumoricidal Activity (% Agent (Reference)supporting

confidence: 85%

“…Macrophage activities differ in dependence on L-arginine. Earlier work with this experimental system has shown that production of NO and N02 and expression of tumoricidal activity were abolished by analogs of L-arginine or arginase, indicating that these two functions depend on L-arginine (30,32,33,35). We have now investigated the extent to which induction by LTAs of the various macrophage activities was affected by the presence of the L-arginine analog, Nmonomethyl-L-arginine (NMMA).…”

Section: -mentioning

confidence: 98%

“…1). The discrepancies in the macrophage (29,30,33) and vascular endothelial (46) systems regarding formation of nitric oxide and expression of biological activity suggested that nitric oxide may not by itself be the critical mediator. Therefore, one must consider the possibility that nitric oxide forms more stable complexes with thiols, iron(II), and/or protein, from which biologically active moieties could be released as required.…”

Section: Tumoricidal Activity (% Agent (Reference)mentioning

confidence: 99%

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Macrophage response to bacteria: induction of marked secretory and cellular activities by lipoteichoic acids

et al. 1992

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Lipoteichoic acids (LTAs) from various bacterial species, including Staphylococcus aureus, Streptococcus pyogenes, Streptococcus pneumoniae, Enterococcusfaecalis, and Listeria monocytogenes, were examined for the ability to induce secretory and cellular responses in a pure population of bone marrow-derived mononuclear phagocytes. Some of the highly purified LTAs, in particular LTAs from Bacilus subtilis, S. pyogenes, E. faecalis, and Enterococcus hirae, were able to affect each of the macrophage parameters measured, i.e., reductive capacity, secretion of tumor necrosis factor and nitrite, and tumoricidal activity. As after stimulation with whole organisms or other bacterial products, secretion of tumor necrosis factor induced by these LTAs reached its maximum within the first few hours of the interaction, while secretion of nitrite and tumoricidal activity required 24 to 36 h for full expression. Other purified LTAs, i.e., LTAs from Streptococcus sanguis, S. pneumoniae, and L. monocytogenes, as well as lipomannan from Micrococcus luteus affected only some of these parameters, while native LTA from S. aureus was inactive. There was no obvious correlation between biological activity and chain length, kind of glycosyl substituents, glycolipid structures, or fatty acid composition of LTAs. Deacylation of LTAs resulted in a complete loss of activity, and deacylated LTAs did not impair the activity of their acylated counterparts, suggesting that acyl chains may be essential for binding of LTA to the cell surface. The results demonstrate that some LTA species are potent inducers of macrophage secretory and cellular activities.

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Section: Tumoricidal Activity (% Agent (Reference)supporting

confidence: 85%

Section: -mentioning

confidence: 98%

Section: Tumoricidal Activity (% Agent (Reference)mentioning

confidence: 99%

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Macrophage response to bacteria: induction of marked secretory and cellular activities by lipoteichoic acids

et al. 1992

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“…mammary gland and macrophages, but there is little or no expression in liver. Rat aortic endothelial cells and murine macrophages express both type I and type II arginases [44,45] and many investigations indicate that both type of arginase have a high activity in activated macrophages [46][47][48][49][50]. Sufficient quantities of arginase can limit the availability of arginine for NO synthesis by intact cells.…”

Section: Effect Of L-arginine On Tumoricidal Activity and Antibacterimentioning

confidence: 99%

Plasmid DNA Vaccines

Abdelnoor

2001

curr drug targets immune endocr metabol disord

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Genes that code for the production of protein antigens have been cloned and recombined with plasmids. Gene-plasmid constructs have been amplified in a bacterial host, purified and administered to a mammalian host. The gene is expressed in the host and the antigen that is produced induces an immune response. These so-called DNA vaccines have been prepared for a number of infectious agents, some tumors and some allergens, and were shown to be efficacious in animal studies. Clinical trials for some of these vaccines are underway. Advantages of using a DNA vaccine include the abilities to favor a T helper-1 or a T helper-2 lymphocyte response and to induce a cytotoxic T-lymphocyte response. Moreover, some reports have indicated that they produce long-lasting immunity. DNA vaccines might be used in situations where no effective vaccine is available for a disease. However, their use might not be risk-free. Further research in this field is needed to determine their efficacy and to identify the risks involved in using them.

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“…Two types of NOS have been identified: one is constitutive and responsible for the physiological transduction purposes and the other is induced by cytokines and releases NO as part of the immunological response [1]. Macrophages [2, 3], Kupffer cells [4] and hepatocytes [5] possess the inducible NOS. Kupffer cells activated by septic stimuli or other inflammatory conditions respond by forming NO themselves and by inducing its formation in neighbouring hepatocytes [6].…”

Section: Introductionmentioning

confidence: 99%

Manipulation of Nitric Oxide in an Animal Model of Acute Liver Injury: The Impact on Liver and Intestinal Function

Adawi¹,

Kasravi²,

Molin³

2007

Libyan J Med

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BackgroundNitric oxide may have a protective effect on the liver during endotoxemia and chronic inflammation. There is evidence that it maintains liver and intestinal tissue integrity during inflammatory processes. We evaluated the impact of altering nitric oxide release on acute liver injury, the associated gut injury and bacterial translocation, at different time intervals.MethodsAn acute rat liver injury model induced by D-galactosamine was used. Sprague Dawley rats were divided into four main groups: normal control, acute liver injury control, acute liver injury + N-nitro-L-arginine methyl ester (L-NAME), acute liver injury + L-NAME + L-arginine. Each group was divided into three subgroups according to the different time intervals (6, 12, 24 hours) after the induction of the liver injury. Liver enzymes and bilirubin were evaluated, as well as bacterial translocation, cecal and colonic microflora, and histological study of liver, ileum and cecum.ResultsLiver enzymes increased significantly at all time intervals in acute liver injury + L-NAME compared to liver injury control groups. Bacterial translocation increased significantly in liver injury + L-NAME groups; at 6 hours to the liver, at 12 hours to the liver and mesenteric lymph nodes (MLNs), and at 24 hours to arterial and portal blood, liver and MLNS. Inhibition of nitric oxide increased significantly the Enterobacteriaceae count in cecum compared to normal and liver injury control groups. The G-negative anaerobes increased significantly in the colon compared to the liver injury control group.ConclusionInhibition of nitric oxide in an acute liver injury model potentiates the liver injury as evidenced by increased appearance of hepatocellular necrosis and elevated liver enzymes and bilirubin. It increases the Enterobacteriaceae in both cecum and colon and Gnegative anaerobes in the colon. It also increases bacterial translocation to extra-intestinal sites. The increased bacterial translocation could be one of the mechanisms potentiating liver injury and nitric oxide may be pathophysiologically involved. Further studies are required to confirm this hypothesis.

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The macrophage response to bacteria: Flow of L-arginine through the nitric oxide and urea pathways and induction of tumoricidal activity

Cited by 24 publications

References 13 publications

Macrophage response to bacteria: induction of marked secretory and cellular activities by lipoteichoic acids

Macrophage response to bacteria: induction of marked secretory and cellular activities by lipoteichoic acids

Plasmid DNA Vaccines

Manipulation of Nitric Oxide in an Animal Model of Acute Liver Injury: The Impact on Liver and Intestinal Function

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