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PubMed2001

Taurine chloramine inhibits inducible nitric oxide synthase and TNF-alpha gene expression in activated alveolar macrophages: decreased NF-kappaB activation and IkappaB kinase activity.

Taurine prevents tissue damage in a variety of models that involve inflammation, including oxidant-induced lung damage. The mechanism of protection is uncertain, but is postulated to involve the actions of taurine chloramine (Tau-Cl) derived via halide-dependent myeloperoxidase associated with neutrophils. Understanding the influence of Tau-Cl on the production of inflammatory mediators by alveolar macrophages provides an opportunity for determining the mechanism of Tau-Cl action. The effects of Tau-Cl were evaluated on the production of NO and TNF-alpha in NR8383, a cloned cell line derived from rat alveolar macrophages (RAM), and in primary cultures of RAM. Production of NO and TNF-alpha, and expression of inducible NO synthase was inhibited by Tau-Cl in activated NR8383 cells as well as in RAM. Temporal (2, 4, 8, 24 h) expression of inducible NO synthase and TNF-alpha mRNAs was reduced by Tau-Cl in NR8383 cells. Tau-Cl depressed NF-kappaB migration into the nucleus of activated NR8383 cells and caused a more sustained presence of IkappaB in the cytoplasm. Stabilization of cytoplasmic IkappaB-alpha in Tau-Cl-treated cells resulted from decreased phosphorylation of IkappaB-alpha serine-32 and a lower activity of IkappaB kinase (IKK). Additional experiments demonstrated that Tau-Cl does not directly inhibit IKK activity. These results suggest that Tau-Cl exerts its effects at some level upstream of IKK in the signaling pathway and inhibits production of inflammatory mediators through a mechanism that, at least in part, involves inhibition of NF-kappaB activation.

Animals↗
PubMed2005

Inhibition of septic arthritis by local administration of taurine chloramine, a product of activated neutrophils.

OBJECTIVE: Taurine is an amino acid able to react with hypochlorous acid, produced endogenously by neutrophils, resulting in the more stable and less toxic taurine chloramine (Tau-Cl). Since Tau-Cl has been shown to down-regulate the production of proinflammatory mediators and to exert anti-bacterial properties, we investigated the efficacy of Tau-Cl treatment for infectious arthritis. METHODS: The murine model of hematogenous septic arthritis involved intravenous injection of a single dose of Staphylococcus aureus. Tau-Cl was administered by daily intraperitoneal injections. In another experiment S. aureus and Tau-Cl were injected intra-articularly. Evaluation of arthritis was performed clinically and histologically. The effect of Tau-Cl on bacterial growth in vitro was also assessed. RESULTS: Growth of staphylococci, including the methicillin-resistant strain 67-0, was inhibited by Tau-Cl. Mice injected with bacteria and Tau-Cl locally in the joint exhibited significantly fewer arthritic lesions. In contrast, there were no obvious differences between Tau-Cl-treated animals and controls with regard to clinical or histological signs of arthritis when bacteria and Tau-Cl were administered systemically. CONCLUSION: Our results show that Tau-Cl exerts an inhibitory effect on the development of bone and cartilage damage in the infected joint when administered intra-articularly.

Animals↗
PubMed1995

Taurine chloramine inhibits production of nitric oxide and TNF-alpha in activated RAW 264.7 cells by mechanisms that involve transcriptional and translational events.

We previously reported that taurine chloramine (Tau-Cl) inhibits the production of both nitric oxide and TNF-alpha by activated RAW 264.7 cells. The current studies were conducted to gain insight into the mechanisms through which Tau-Cl exerts these effects. RAW 264.7 cells were activated by LPS (10 micrograms/ml) and rIFN-gamma (50 U/ml) in the absence or presence of either 0.8 mM Tau-Cl or taurine. Production of NO and TNF-alpha by RAW 264.7 cells was monitored: NO was measured spectrophotometrically as nitrite and TNF-alpha was measured by ELISA. Cell lysates were analyzed for the inducible form of nitric oxide synthase (iNOS) by Western blot analyses, and TNF-alpha and iNOS mRNAs were assessed by northern blot analyses. Tau-Cl inhibited transcription of the iNOS gene, or some earlier event in the signal transduction pathway, because iNOS protein and iNOS mRNA were undetected in lysates of cells activated in the continuous presence of Tau-Cl. In contrast, steady-state levels of TNF-alpha mRNA increased in the presence of Tau-Cl to at least the same extent as that in untreated activated cells and persisted for a longer period of time. Metabolic labeling experiments demonstrated that Tau-Cl inhibited translation of TNF-alpha mRNA because the presence of the presecretory 26-kDa form and the secreted 17-kDa form of TNF-alpha were greatly reduced in lysates and culture media, respectively, of cells activated in the presence of Tau-Cl. Inhibition of TNF-alpha synthesis by Tau-Cl is not the result of a generalized effect on protein synthesis because the amount of radiolabeled protein precipitated from metabolically labeled cells by TCA was unaffected by Tau-Cl, and cell viability was unaffected. The results of these studies demonstrate that Tau-Cl decreases production of tissue-damaging inflammatory mediators and thus may act as a physiologic modulator of macrophage function.

Amino Acid Oxidoreductases↗