The mechanism of taurine chloramine inhibition of cytokine (interleukin‐6, interleukin‐8) production by rheumatoid arthritis fibroblast‐like synoviocytes

Kontny, Ewa; Szczepańska, Katarzyna; Kowalczewski, Jacek; Kurowska, Weronika; Janicka, Iwona; Marcinkiewicz, Janusz; Maśliński, Włodzimierz

doi:10.1002/1529-0131(200010)43:10<2169::aid-anr4>3.0.co;2-#

Cited by 93 publications

(52 citation statements)

References 47 publications

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“…22,[24][25][26] Taurine is also known to have potent antioxidant properties and to regulate proinflammatory cytokines. [27][28][29] Although taurine has proven effective for treating alcohol-induced hepatic injury, 30 the precise signaling involved in its protective activity is still unclear. This study further showed that by inhibiting TLR-4/ MyD88 and IjB/NFjB p65 signaling, taurine suppresses inflammation-associated proteins and cytokines, which alleviates chronic alcohol-induced liver inflammation.…”

Section: Discussionmentioning

confidence: 99%

Taurine Attenuates Hepatic Inflammation in Chronic Alcohol-Fed Rats Through Inhibition of TLR4/MyD88 Signaling

Lin

Chiu

Chen

et al. 2015

Journal of Medicinal Food

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Accumulating evidence indicates that overconsumption of ethanol contributes in many ways to the pathogenesis of hepatic injury. Although studies indicate that taurine decreases lipogenesis, oxidative stress, and inflammatory cytokines, the protective effect of taurine against alcohol-induced liver injury is still unclear. To clarify the precise signaling involved in the beneficial effect of taurine on alcohol-induced liver injury, rats were randomly divided into four treatment groups: (1) control (Ctl), (2) alcohol (Alc), (3) Alc + taurine (Tau), and (4) Alc + silymarin (Sil). The Tau and Sil groups had lower lymphocyte infiltration and significantly lower TLR-4/MyD88 and IjB/NFjB compared to the Alc group. The inducible nitric oxide synthase (iNOS), C-reactive protein (CRP), tumor necrosis factors (TNF)-a, interleukin (IL)-6, and IL-1b were also significantly lower in the Tau and Sil groups than in the Alc group. The experimental results indicated that hepatoprotection against alcohol-induced inflammation may be mediated by decreased TLR-4/MyD88 signaling.

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Section: Discussionmentioning

confidence: 99%

Taurine Attenuates Hepatic Inflammation in Chronic Alcohol-Fed Rats Through Inhibition of TLR4/MyD88 Signaling

Lin

Chiu

Chen

et al. 2015

Journal of Medicinal Food

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“…After 18 h of treatment, total RNA was prepared and transcribed into complementary DNA (cDNA) as described previously [26]. The selection of this optimal time point for RNA analysis was based on preliminary time course (6-24 h) experiments.…”

Section: Reverse Transcriptase-polymerase Chain Reaction (Rt-pcr)mentioning

confidence: 99%

“…It is possible that the blockade of RA FLS cell-cycle progression may represent novel therapeutic approach for RA treatment. We have previously found that taurine chloramine (Tau-Cl), a physiologic compound of known anti-infl ammatory activities, inhibits not only some pro-infl ammatory functions of RA FLS [25][26][27][28][29] but also proliferation of these cells [25,29]. Taurine chloramine is generated by activated neutrophils in a reaction of hypochlorous acid (HOCl) with b-amino acid taurine (Tau) [30].…”

Section: Introductionmentioning

confidence: 99%

Taurine chloramine inhibits proliferation of rheumatoid arthritis synoviocytes by triggering a p53-dependent pathway

Kontny¹,

Rudnicka²,

Chorąży-Massalska³

et al. 2006

Inflamm. res.

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“…36) or IL-15DM/Fc␥1 (human Fc␥1), a high-affinity receptor site-specific antagonist for IL-15R␣-chain protein (both from Cardion Pharmaceuticals, Boston, MA); 2) relevant isotype controls, murine IgG2a or human IgG1, respectively (both Abs from R&D Systems); 3) goat anti-human IL-15 neutralizing Ab (5 g/ml); or 4) control total goat IgG (both Abs from R&D Systems). After 24 h, one-third of the culture medium was discarded and fresh medium with supplementary proteins were added for another 24 h. Total RNA extraction, cDNA template preparation, and the RT-PCR were done as previously described (37). Quantitative competitive RT-PCR was used to measure bcl-2, bcl-x L , and GAPDH mRNA expression.…”

Section: Expression Of Mrna-encoding Il-15 Il-15r␣ Il-2/il-15r␤ Ilmentioning

confidence: 99%

Fibroblast-Like Synoviocytes from Rheumatoid Arthritis Patients Express Functional IL-15 Receptor Complex: Endogenous IL-15 in Autocrine Fashion Enhances Cell Proliferation and Expression of Bcl-xL and Bcl-2

Kurowska¹,

Rudnicka²,

Kontny³

et al. 2002

The Journal of Immunology

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101

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The hallmarks of rheumatoid arthritis (RA) are leukocytic infiltration of the synovium and expansiveness of fibroblast-like synoviocytes (FLS). The abnormal proliferation of FLS and their resistance to apoptosis is mediated, at least in part, by present in RA joints proinflammatory cytokines and growth factors. Because IL-15 exerts properties of antiapoptotic and growth factors, and is produced by RA FLS, we hypothesized that IL-15 participates in RA FLS activation. To test this hypothesis, we first examined whether RA FLS express chains required for high affinity functional IL-15R. Indeed, RA FLS express IL-15Rα at mRNA and protein levels. Moreover, we confirmed the presence of IL-2Rβ and common γ-chains. Interestingly, TNF-α or IL-1β triggered significant elevation of IL-15Rα chain at mRNA and protein levels. Next, we investigated the effects of exogenous or endogenous IL-15 on Bcl-2 and Bcl-xL expression, FLS proliferation, and apoptosis. Exogenous IL-15 enhanced RA FLS proliferation and increased the level of mRNA-encoding Bcl-xL. To test the role of endogenous IL-15 in the activation of RA FLS, an IL-15 mutant/Fcγ2a protein exerting properties of specific antagonist to the IL-15Rα chain was used. We found that blocking IL-15 biological activities using this protein substantially reduced endogenous expression of Bcl-2 and Bcl-xL, and RA FLS proliferation that was reflected by increased apoptosis. Thus, we have demonstrated that a distinctive phenotype of RA FLS, i.e., persistent activation, proliferation, and resistance to apoptosis, is related to the autocrine activation of IL-15Rs by FLS-derived IL-15.

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The mechanism of taurine chloramine inhibition of cytokine (interleukin‐6, interleukin‐8) production by rheumatoid arthritis fibroblast‐like synoviocytes

Abstract: Tau-Cl inhibition of IL-6 and IL-8 synthesis in FLS from RA patients results from the ability of this compound to diminish the activity of the major transcriptional regulators (NF-kappaB and AP-1), which subsequently reduces the transcription of these cytokine genes.

Cited by 93 publications

References 47 publications

Taurine Attenuates Hepatic Inflammation in Chronic Alcohol-Fed Rats Through Inhibition of TLR4/MyD88 Signaling

Taurine Attenuates Hepatic Inflammation in Chronic Alcohol-Fed Rats Through Inhibition of TLR4/MyD88 Signaling

Taurine chloramine inhibits proliferation of rheumatoid arthritis synoviocytes by triggering a p53-dependent pathway

Fibroblast-Like Synoviocytes from Rheumatoid Arthritis Patients Express Functional IL-15 Receptor Complex: Endogenous IL-15 in Autocrine Fashion Enhances Cell Proliferation and Expression of Bcl-xL and Bcl-2

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