Taurine chloramine down-regulates the generation of murine neutrophil inflammatory mediators

Marcinkiewicz, Janusz; Grabowska, Agnieszka; Bereta, Joanna; Bryniarski, Krzysztof; Nowak, Bernadeta

doi:10.1016/s0162-3109(98)00023-x

Cited by 91 publications

(65 citation statements)

References 33 publications

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“…Moreover, the macrophages of taut Ϫ/Ϫ mice appear to change their stability in response to malaria, as circumstantially indicated by the increased systemic levels of TNF-␣ and IL-1␤, which are produced primarily by macrophages. This accords with other data showing, conversely, that taurine is able to dampen the effect of proinflammatory cytokines, including IL-1␤ (12) and TNF-␣ (10,24,33,34,44,47,60).…”

Section: Discussionsupporting

confidence: 92%

Loss of Ability To Self-Heal Malaria upon Taurine Transporter Deletion

et al. 2010

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Deletion of the taurine transporter gene (taut) results in lowered levels of taurine, the most abundant amino acid in mammals. Here, we show that taut ؊/؊ mice have lost their ability to self-heal blood-stage infections with Plasmodium chabaudi malaria. All taut ؊/؊ mice succumb to infections during crisis, while about 90% of the control taut ؉/؉ mice survive. The latter retain unchanged taurine levels even at peak parasitemia. Deletion of taut, however, results in the lowering of circulating taurine levels from 540 to 264 mol/liter, and infections cause additional lowering to 192 mol/liter. Peak parasitemia levels in taut ؊/؊ mice are approximately 60% higher than those in taut ؉/؉ mice, an elevation that is associated with increased systemic tumor necrosis factor alpha (TNF-␣) and interleukin-1␤ (IL-1␤) levels, as well as with liver injuries. The latter manifest as increased systemic ammonia levels, a perturbed capacity to entrap injected particles, and increased expression of genes encoding TNF-␣, IL-1␤, IL-6, inducible nitric oxide synthase (iNOS), NF-B, and vitamin D receptor (VDR). Autopsy reveals multiorgan failure as the cause of death for malaria-infected taut ؊/؊ mice. Our data indicate that taut-controlled taurine homeostasis is essential for resistance to P. chabaudi malaria. Taurine deficiency due to taut deletion, however, impairs the eryptosis of P. chabaudi-parasitized erythrocytes and expedites increases in systemic TNF-␣, IL-1␤, and ammonia levels, presumably contributing to multiorgan failure in P. chabaudi-infected taut ؊/؊ mice.

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Section: Discussionsupporting

confidence: 92%

Loss of Ability To Self-Heal Malaria upon Taurine Transporter Deletion

et al. 2010

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“…The injection volume was 10 l. The ion spray voltage was 4,500 V, and nitrogen was the only gas used throughout the runs. Standard Cl-tau was prepared as described earlier (24). In brief, 20 mM HOCl in 100 mM potassium phosphate buffer (pH 7.4) was added in equal volumes of 100 mM taurine with vigorous stirring.…”

Section: Methodsmentioning

confidence: 99%

Microbicidal Activity of Vascular Peroxidase 1 in Human Plasma via Generation of Hypochlorous Acid

Cao

Moore

et al. 2012

Infect Immun

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ABSTRACTMembers of the heme peroxidase family play an important role in host defense. Myeloperoxidase (MPO) is expressed in phagocytes and is the only animal heme peroxidase previously reported to be capable of using chloride ion as a substrate to form the highly microbicidal species hypochlorous acid (HOCl) at neutral pH. Despite the potent bacterial killing activity of HOCl, individuals who fail to express MPO typically show only a modest increase in some fungal infections. This may point to the existence of redundant host defense mechanisms. Vascular peroxidase 1 (VPO1) is newly discovered member of the heme peroxidase family. VPO1 is expressed in cells of the cardiovascular system and is secreted into the bloodstream. In the present study, we investigate whether VPO1 is capable of generating HOCl and its role in host defense. Like MPO, VPO1 in the presence of H2O2and chloride generates HOCl. VPO1-dependent HOCl generation was demonstrated by chlorination of taurine and tyrosine using mass spectrometry. In addition, the VPO1/H2O2/Cl−system can cause the chlorination of monochlorodimedone and the oxidation of 5-thio-2-nitrobenzoic acid. Purified VPO1 and VPO1 in plasma mediate bacterial killing that is dependent on chloride and H2O2; killing is inhibited by peroxidase inhibitors and by the H2O2scavenger catalase. In the presence of erythrocytes, bacterial killing by VPO1 is slightly reduced. Thus, VPO1, in addition to MPO, is the second member of the heme peroxidase family capable of generating HOCl under physiological conditions. VPO1 is likely to participate in host defense, with bactericidal activity mediated through the generation of HOCl.

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“…Taurine did not at all affect NFDL expression by TNF (data not shown). Because it is known that TauCl is produced at sites of inflammation by the reaction of taurine with HOCl generated from MPO (Stapleton et al, 1998) and plays a role as a negative regulator of inflammation (Marcinkiewicz et al, 1998), it was thought that the taurine effect may be through formation of TauCl in the inflamed colonic tissue. Although MPO activity of inflamed colonic tissue is much greater than that of normal colonic tissue, it is not clear whether TauCl could be formed from exogenous taurine in the inflamed colon.…”

Section: Resultsmentioning

confidence: 99%

“…The reaction occurs physiologically around or in activated immune cells that contain a large amount of taurine to protect tissues from the highly toxic effect of HOCl/OCl Ϫ (Schuller- Levis et al, 1994). An expanding body of evidence suggests that taurine chloramine plays an important role in inflammatory progression by modulating NF-B activity and attenuating production of proinflammatory mediators such as prostaglandins, nitric oxide, and cytokines (Marcinkiewicz et al, 1998;Barua et al, 2001).…”

mentioning

confidence: 99%

A Molecular Mechanism for the Anti-Inflammatory Effect of Taurine-Conjugated 5-Aminosalicylic Acid in Inflamed Colon

Kim¹,

Jeon²,

Kong³

et al. 2006

Mol Pharmacol

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In previous reports, a novel colon-specific prodrug, 5-aminosalicyltaurine (5-ASA-Tau) administered orally, is successfully delivered to and liberates 5-aminosalicylic acid (5-ASA) and taurine in the inflamed large intestine of rats. Furthermore, the prodrug ameliorates the 2,4,6-trinitrobenzene-sulfonic acid-induced colitis, and taurine acts not only as a carrier but also as an active therapeutic agent. In this study, we investigated the anti-inflammatory properties of the prodrug at a molecular level. After rectal administration of taurine, formation of taurine chloramine (TauCl) in the inflamed colonic tissue was examined using high-performance liquid chromatography. In human colon epithelial cell lines, nuclear factor-B (NF-B) activity was accessed using an NF-B-dependent luciferase reporter gene. Protein levels were monitored by Western blotting. DNA binding activity of the NF-B subunit p65 was determined using a DNA binding assay kit. A millimolar level of TauCl was formed in the inflamed tissue. TauCl inhibited tumor necrosis factor (TNF)-dependent NF-B activation by modifying thiol(s) on p65 and blocking DNA binding. In addition, 5-ASA inhibited phosphorylation of p65 at serine 536, which is critical for transcriptional activity of NF-B. Furthermore, combined TauCl/5-ASA treatment additively inhibited TNF-dependent NF-B activation. Together, our data suggest that the colon-specific carrier taurine contributes to the clinical effect of the prodrug by potentiating the inhibitory effect of the active ingredient 5-ASA on a major proinflammatory signal, TNF-dependent NF-B activation in the inflamed large intestine.

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Taurine chloramine down-regulates the generation of murine neutrophil inflammatory mediators

Cited by 91 publications

References 33 publications

Loss of Ability To Self-Heal Malaria upon Taurine Transporter Deletion

Loss of Ability To Self-Heal Malaria upon Taurine Transporter Deletion

Microbicidal Activity of Vascular Peroxidase 1 in Human Plasma via Generation of Hypochlorous Acid

A Molecular Mechanism for the Anti-Inflammatory Effect of Taurine-Conjugated 5-Aminosalicylic Acid in Inflamed Colon

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