Elastin receptor (Spliced galactosidase) occupancy by elastin peptides counteracts proinflammatory cytokine expression in lipopolysaccharide-stimulated NF-κB down-regulation

被引:35
|
作者
Baranek, Thomas
Debret, Romain
Antonicelli, Frank
Lamkhioued, Bouchaib
Belaaouaj, Azzaq
Hornebeck, William
Bernard, Philippe
Guenounou, Moncef
Le Naour, Richard
机构
[1] Lab Immunol & Microbiol, Unite Format & Rech Pharm, EA3796, IFR53, F-51096 Reims, France
[2] CNRS, Lab Biochim & Dermatol, UMR 6198, Unite Format & Rech Med, Reims, France
[3] Ctr Hosp Univ Maison Blanche, Inst Natl Sante & Rech Med, UMR Sante 514, Reims, France
来源
JOURNAL OF IMMUNOLOGY | 2007年 / 179卷 / 09期
关键词
D O I
10.4049/jimmunol.179.9.6184
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
In inflammatory diseases, strong release of elastinolytic proteases results in elastin fiber degradation generating elastin peptides (EPs). Chernotactic activity for inflammatory cells was, among wide range of properties, the former identified biological activity exerted by EPs. Recently, we demonstrated the ability of EPs to favor a Th1 cytokine (IL-2, IFN-gamma) cell response in lymphocytes and to regulate IL-1 beta expression in melanoma cells. We hypothesized that EPs might also influence inflammatory cell properties by regulating cytokine expression by these cells. Therefore, we investigated the influence of EPs on inflammatory cytokine synthesis by human monocytes. We evidenced that EPs down-regulated both at the mRNA and protein levels the proinflammatory TNF-alpha, IL-1 beta, and IL-6 expression in LPS-activated monocytes. Such negative feedback loop could be accounted solely for EP-mediated effects on proinflammatory cytokine production because EPs did not affect anti-inflammatory IL-10 or TGF-beta secretion by LPS-activated monocytes. Furthermore, we demonstrated that EP effect on proinflammatory cytokine expression by LPS-stimulated monocytes could not be due either to a decrease of LPS receptor expression or to an alteration of LPS binding to its receptor. The inhibitory effects of EPs on cytokine expression were found to be mediated by receptor (spliced galactosidase) occupancy, as being suppressed by lactose, and to be associated with the decrease of NF-kappa B-DNA complex formation. As a whole, these results demonstrated that EP/spliced galactosidase interaction on human monocytes down-regulated NF-kappa B-dependent proinflammatory cytokine expression and pointed out the critical role of EPs in the regulation of inflammatory response.
引用
收藏
页码:6184 / 6192
页数:9
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