Plasma nitrate concentration in infective gastroenteritis and inflammatory bowel disease.

Dykhuizen, R S; Masson, Jean‐Bernard; McKnight, G. M.; Mowat, A. N. G.; Smith, C. C.; Smith, Lorna; Benjamin, Nigel

doi:10.1136/gut.39.3.393

Cited by 60 publications

(36 citation statements)

References 17 publications

(3 reference statements)

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“…Studies in experimental animals also suggest a beneficial role of inducible NO synthase during Salmonella infection (25), and elevated production of NO has been detected in patients with bacterial gastroenteritis (29). The present observations indicate that synergistic antimicrobial activity can result from the combination of the phagocyte respiratory burst and NO synthase in vivo as well as in vitro.…”

Section: Discussionsupporting

confidence: 70%

Periplasmic superoxide dismutase protectsSalmonellafrom products of phagocyte NADPH-oxidase and nitric oxide synthase

Groote

Ochsner

Shiloh

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

362

345

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Superoxide dismutase (SOD) catalyzes the conversion of superoxide radical to hydrogen peroxide. Periplasmic localization of bacterial Cu,Zn-SOD has suggested a role of this enzyme in defense against extracellular phagocyte-derived reactive oxygen species. Sequence analysis of regions f lanking the Salmonella typhimurium sodC gene encoding Cu,Zn-SOD demonstrates significant homology to phage proteins, ref lecting possible bacteriophage-mediated horizontal gene transfer of this determinant among pathogenic bacteria. Salmonella deficient in Cu,Zn-SOD has reduced survival in macrophages and attenuated virulence in mice, which can be restored by abrogation of either the phagocyte respiratory burst or inducible nitric oxide synthase. Moreover, a sodC mutant is extremely susceptible to the combination of superoxide and nitric oxide. These observations suggest that SOD protects periplasmic or inner membrane targets by diverting superoxide and limiting peroxynitrite formation, and they demonstrate the ability of the respiratory burst and nitric oxide synthase to synergistically kill microbial pathogens in vivo.

show abstract

Section: Discussionsupporting

confidence: 70%

Periplasmic superoxide dismutase protectsSalmonellafrom products of phagocyte NADPH-oxidase and nitric oxide synthase

Groote

Ochsner

Shiloh

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

362

345

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“…During this phase, NO provides microbicidal activity in concert with the relatively potent phagocyte respiratory burst. The role of NO in human host defense against Salmonella serovar Typhimurium is far less clear, but elevated production of NO has been detected in patients with bacterial gastroenteritis (10). Although most investigators have demonstrated NO production by human macrophages (43), the role of NO in the microbicidal activity of human macrophages remains controversial.…”

Section: Discussionmentioning

confidence: 99%

Flavohemoglobin Hmp ProtectsSalmonella entericaSerovar Typhimurium from Nitric Oxide-Related Killing by Human Macrophages

et al. 2002

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Survival of macrophage microbicidal activity is a prerequisite for invasive disease caused by the enteric pathogen Salmonella enterica serovar Typhimurium. Flavohemoglobins, such as those of Escherichia coli, Salmonella, and yeast, play vital roles in protection of these microorganisms in vitro from nitric oxide (NO) and nitrosative stress. A Salmonella hmp mutant defective in flavohemoglobin (Hmp) synthesis exhibits growth that is hypersensitive to nitrosating agents. We found that respiration of this mutant exhibited increased inhibition by NO, whereas wild-type cells pregrown with sodium nitroprusside or S-nitrosoglutathione showed enhanced tolerance of NO. Most significantly, hmp mutants internalized by primary human peripheral monocyte-derived macrophages survived phagocytosis relatively poorly compared with similarly bound and internalized wild-type cells. That the enhanced sensitivity to macrophage microbicidal activity is due primarily to the failure of Salmonella to detoxify NO was suggested by the ability of L-N G -monomethyl arginine-an inhibitor of NO synthase-to eliminate the difference in killing between wild-type and hmp mutant Salmonella cells. These observations suggest that Salmonella Hmp contributes to protection from NO-mediated inhibition by human macrophages.

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“…Humans unquestionably produce dramatically elevated quantities of NO during infection and other inflammatory conditions (4,24). Nevertheless, in vitro treatment of human peripheral blood mononuclear cells with lipopolysaccharide and interferon-␥ fails to elicit NO production (15), even though these stimuli are highly effective in provoking murine macrophages to generate copious quantities of NO (19).…”

mentioning

confidence: 99%

Nitric oxide production by human macrophages: there's NO doubt about it

Fang

Vázquez‐Torres

2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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Plasma nitrate concentration in infective gastroenteritis and inflammatory bowel disease.

Cited by 60 publications

References 17 publications

Periplasmic superoxide dismutase protectsSalmonellafrom products of phagocyte NADPH-oxidase and nitric oxide synthase

Periplasmic superoxide dismutase protectsSalmonellafrom products of phagocyte NADPH-oxidase and nitric oxide synthase

Flavohemoglobin Hmp ProtectsSalmonella entericaSerovar Typhimurium from Nitric Oxide-Related Killing by Human Macrophages

Nitric oxide production by human macrophages: there's NO doubt about it

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