Taurine chloramine, a product of activated neutrophils, inhibits in vitro the generation of nitric oxide and other macrophage inflammatory mediators

Taurine (Tau) is an exceptionally abundant free amino acid in the cytosol of inflammatory cells and especially in neutrophils. Taurine protects cells from self‐destruction during processes that generate oxidants. The major function of Tau in leukocytes is to trap chlorinated oxidants (HOCl). Taurine...

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Bibliographic Details
Published in:Journal of leukocyte biology 1995-12, Vol.58 (6), p.667-674
Main Authors: Marcinkiewicz, Janusz, Grabowska, Agnieszka, Bereta, Joanna, Stelmaszynska, Teresa
Format: Article
Language:English
Subjects:
Animals
Cells, Cultured
Cytokines - biosynthesis
Dinoprostone - biosynthesis
Inflammation Mediators - metabolism
interleukin‐1α
interleukin‐6
macrophages
Macrophages - drug effects
Macrophages - metabolism
Male
Mice
Mice, Inbred CBA
Neutrophil Activation
neutrophils
Neutrophils - physiology
nitric oxide
Nitric Oxide - biosynthesis
Nitric Oxide Synthase - genetics
prostaglandin E2
RNA, Messenger - analysis
taurine
Taurine - analogs & derivatives
Taurine - pharmacology
tumor necrosis factor α
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Summary:Taurine (Tau) is an exceptionally abundant free amino acid in the cytosol of inflammatory cells and especially in neutrophils. Taurine protects cells from self‐destruction during processes that generate oxidants. The major function of Tau in leukocytes is to trap chlorinated oxidants (HOCl). Taurine reacts with HOCl to produce the long‐lived compound taurine chloramine (TauCl). Previously, we have shown that other products of the neutrophil chlorinating system are able to modify functions of macrophages. In this study, we investigated in vitro the influence of TauCl on the generation of inflammatory mediators by activated macrophages. We have found that TauCl inhibited the generation of nitric oxide, prostaglandin E2, tumor necrosis factor α, and interleukin‐6, but TauCl slightly enhanced the release of IL‐1α. The formation of nitrites by interferon‐γ‐activated macrophages was inhibited by TauCl in a dose‐dependent manner. Taurine chloramine also reduced the level of inducible nitric oxide synthase (iNOS) mRNA in macrophages, in a similar concentration‐dependent manner. Although our experiments do not exclude a direct effect of TauCl on enzymatic activity of iNOS, the inhibition of iNOS expression seems to be the major mechanism responsible for suppression of NO formation. Finally, we discuss the biological role of TauCl in vivo. We suggest that at the site of inflammation TauCl works as a specific signaling molecule of activated neutrophils that coordinates the generation of inflammatory mediators in macrophages.
ISSN:0741-5400
1938-3673
DOI:10.1002/jlb.58.6.667