Glucocorticoid-mediated Gene Suppression of Rat Cytokine-induced Neutrophil Chemoattractant CINC/gro, a Member of the Interleukin-8 Family, through Impairment of NF-κB Activation

Ohtsuka, Toshiaki; Kubota, Akira; Hirano, Takae; Watanabe, Kimitsuna; Yoshida, Hiroyuki; Tsurufuji, M; Iizuka, Yoshio; Kawai, Kiyoshi; Tsurufuji, Susumu

doi:10.1074/jbc.271.3.1651

Cited by 103 publications

(58 citation statements)

References 56 publications

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“…Male Brown Norway rats (Seakku-Yoshitomi, Fukuoka, Japan) 6 -8 wk old and weighing ϳ250 g were used for the study. A C5a receptor antagonist (C5a hexapeptide; NMePhe-Lys-Pro-dCha-Trp-dArg) and rat cytokine-induced neutrophil chemoattractant-1 (CINC-1) were purchased from the Peptide Institute (Osaka, Japan) (22,23). sCR1 and Futhan were donated by Avant Immunotherapeutics (Needham, MA) and Torii Pharmaceutical (Osaka, Japan), respectively.…”

Section: Methodsmentioning

confidence: 99%

Contribution of Anaphylatoxin C5a to Late Airway Responses After Repeated Exposure of Antigen to Allergic Rats

Abe¹,

Shibata

Akatsu

et al. 2001

The Journal of Immunology

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We attempted to elucidate the contribution of complement to allergic asthma. Rat sensitized to OVA received repeated intratracheal exposures to OVA for up to 3 consecutive days, and pulmonary resistance was then estimated for up to 6 h after the last exposure. Whereas the immediate airway response (IAR) in terms of RL tended to decrease in proportion to the number of OVA exposures, late airway response (LAR) became prominent only after three. Although premedication with two kinds of complement inhibitors, soluble complement receptor type 1 (sCR1) or nafamostat mesylate, resulted in inhibition of the IAR after either a single or a double exposure, the LAR was inhibited after the triple. Premedication with a C5a receptor antagonist (C5aRA) before every exposure to OVA also inhibited the LAR after three. Repeated OVA exposure resulted in eosinophil and neutrophil infiltration into the bronchial submucosa which was suppressed by premedication with sCR1 or C5aRA. Up-regulation of C5aR mRNA was shown in lungs after triple OVA exposure, but almost no up-regulation of C3aR. Pretreatment with sCR1 or C5aRA suppressed the up-regulation of C5aR expression as well as cytokine messages in the lungs. The suppression of LAR by pretreatment with sCR1 was reversed by intratracheal instillation of rat C5a desArg the action of which was inhibited by C5aRA. In contrast, rat C3a desArg or cytokine-induced neutrophil chemoattractant-1 induced cellular infiltration into the bronchial submucosa by costimulation with OVA, but these had no influence on the LAR. These differences might be explained by the fact that costimulation with OVA and C5a synergistically potentiated IAR, whereas that with OVA and either C3a or cytokine-induced neutrophil chemoattractant-1 did not. C5a generated by Ag-Ab complexes helps in the production of cytokines and contributes to the LAR after repeated exposure to Ag.

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Section: Methodsmentioning

confidence: 99%

Contribution of Anaphylatoxin C5a to Late Airway Responses After Repeated Exposure of Antigen to Allergic Rats

Abe¹,

Shibata

Akatsu

et al. 2001

The Journal of Immunology

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“…Sasaki et al [29] reported that in rats with dextran sodium sulphate induced-colitis, CINC-1 production increased in the proximal large intestine; moreover, this effect was reversed by rectally injected prostaglandin E2. In the normal rat kidney epithelial cell line (NRK-52E), IL-1β, LPS, or TNF-α stimulation resulted in the production of CINC-1 (at 5 h) as well as CINC-1 mRNA expression (maximum at 3 h) [30]. Campbell et al [31] reported a complex mechanism of CINC-1 production, namely, they found that IL-1β microinjection into the rat striatum in the brain using a minimally invasive traumatic technique resulted in a significant increase in hepatic CINC-1 mRNA expression and serum CINC-1 production in a dose-dependent manner 2 h after injection of IL-1β into the striatum.…”

Section: Agents or Conditions That Induce Cinc-1 Productionmentioning

confidence: 99%

“…Ohtsuka et al [30] further investigated the importance of NFκB in CINC-1 production. Their nuclear run-on assays revealed that CINC-1 gene expression in a IL-1β-stimulated normal rat kidney epithelial cell line (NRK-52E) is regulated at the transcriptional level.…”

Section: Nuclear Factor Kappa B (Nfκb)-mediated Transcription In Cincmentioning

confidence: 99%

“…Other transcriptional factors such as activator protein-1 (AP-1) [11] and NF-IL6 [30] have also been investigated in this context. Deletion of the NF-IL6 binding site was found to have little effect on CINC-1 gene activation, whereas the deletion or mutation of the NFκB binding site abolished IL-1β-induced CINC-1 gene activation; these results suggested that the NFκB binding site plays an essential role in CINC-1 gene activation by IL-1β.…”

Section: Nuclear Factor Kappa B (Nfκb)-mediated Transcription In Cincmentioning

confidence: 99%

“…Ohtsuka et al [30] investigated the suppressive effects of dexamethasone on IL-1β-induced CINC-1 production by a normal rat kidney cell line (NRK52E). They demonstrated that the effects of dexamethasone are the result of an inhibition of NFκB (p65 subunit) translocation from the cytoplasm into the nucleus, and not the result of an inhibition of IκB degradation.…”

Section: Other Agents That Suppress Cinc-1 Productionmentioning

confidence: 99%

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Rat Cytokine-Induced Neutrophil Chemoattractant-1 (CINC-1) in Inflammation

Handa¹,

Naito²,

Yoshikawa³

2006

J. Clin. Biochem. Nutr.

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Summary Rat cytokine-induced neutrophil chemoattractant-1 (CINC-1) belongs to the CXCchemokine family and is a counterpart of human growth-related oncogene (GRO) in the interleukin-8 (IL-8) family. In rats, CINC-1 plays a key role in neutrophil-mediated inflammatory diseases by attracting neutrophils to the site of inflammation. Although IL-8 is a well-known chemokine in humans, it remains difficult to investigate human inflammatory diseases in detail. Therefore CINC-1 is expected to be an excellent tool for investigating neutrophil-mediated inflammatory diseases, and it has served extensively as a target chemokine in studies performed to date. However, little is known regarding CINC-1 signaling pathways. In this review, we focused on the signal transduction of CINC-1 production/ expression.

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Enhanced expression of cytokine-induced neutrophil chemoattractant in rat hepatic allografts during acute rejection

et al. 1997

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The kinetics of messenger RNA (mRNA) and protein levels of cytokine-induced neutrophil chemoattractant (CINC) in rat hepatic allografts during acute rejection were investigated. Infiltrating cells were identified by double immunostaining with anti-CINC and anti-macrophage monoclonal antibodies, ED1 and ED2. The serum CINC concentration in untreated hepatic allograft recipients increased significantly at a constant rate over time after transplantation. No significant increases in serum CINC concentrations were observed in hepatic isografts or allografts treated with the immunosuppressant FK506. The number of neutrophils in untreated hepatic allografts increased significantly at a constant rate. Conversely, neutrophil accumulation in isografts or allografts treated with FK506 was much less than in untreated hepaticallografts. Immunostaining revealed that in the portal areas, mononuclear cells infiltrating untreated allograft liver were mainly positive for CINC and that CINC+ cells represented a subpopulation (approximately 25%) of the ED1+ cells. On the other hand, in the sinusoidal areas CINC+ cells were scattered and mainly positive for ED2. Levels of CINC mRNA in liver tissues taken from untreated hepatic allografts increased after transplantation, peaked on day 5, and decreased thereafter. Hepatic allografts treated with FK506 or isografts showed much lower levels of CINC mRNA than untreated allografts. Allogeneic mixed lymphocyte reactions induced CINC production. The cellular source of CINC was mononuclear cells. CINC production in mixed lymphocyte reactions was inhibited in the presence of anti-tumor necrosis factor alpha (TNF-alpha) antibody. These results suggest that enhanced expression of CINC mRNA and prominent accumulation of neutrophils in the liver grafts are characteristic features of the immune response during acute rejection.

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Glucocorticoid-mediated Gene Suppression of Rat Cytokine-induced Neutrophil Chemoattractant CINC/gro, a Member of the Interleukin-8 Family, through Impairment of NF-κB Activation

Cited by 103 publications

References 56 publications

Contribution of Anaphylatoxin C5a to Late Airway Responses After Repeated Exposure of Antigen to Allergic Rats

Contribution of Anaphylatoxin C5a to Late Airway Responses After Repeated Exposure of Antigen to Allergic Rats

Rat Cytokine-Induced Neutrophil Chemoattractant-1 (CINC-1) in Inflammation

Enhanced expression of cytokine-induced neutrophil chemoattractant in rat hepatic allografts during acute rejection

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