Cutting Edge: IL-6 Is a Marker of Inflammation with No Direct Role in Inflammasome-Mediated Mouse Models

被引：84

作者：

McGeough, Matthew D. ^{[1
]}

Pena, Carla A. ^{[1
]}

Mueller, James L. ^{[1
,2
]}

Pociask, Derek A. ^{[3
]}

Broderick, Lori ^{[4
,5
]}

Hoffman, Hal M. ^{[1
,2
,4
,5
]}

Brydges, Susannah D. ^{[1
]}

机构：

[1] Univ Calif San Diego, Dept Pediat, La Jolla, CA 92093 USA

[2] Ludwig Inst Canc Res, San Diego Branch, La Jolla, CA 92093 USA

[3] Univ Pittsburgh, Childrens Hosp Pittsburgh, Med Ctr, Pediat Res Inst,Richard King Mellon Fdn, Pittsburgh, PA 15224 USA

[4] Univ Calif San Diego, Div Rheumatol Allergy & Immunol, La Jolla, CA 92093 USA

[5] Rady Childrens Hosp San Diego, San Diego, CA 92123 USA

来源：

JOURNAL OF IMMUNOLOGY | 2012年 / 189卷 / 06期

基金：

新加坡国家研究基金会; 美国国家卫生研究院;

关键词：

INTERLEUKIN 6-DEFICIENT MICE; COLD AUTOINFLAMMATORY SYNDROME; MUCKLE-WELLS-SYNDROME; INTERLEUKIN-6-DEFICIENT MICE; INTESTINAL INFLAMMATION; EXPERIMENTAL ARTHRITIS; ARTICULAR SYNDROME; IMMUNE-RESPONSE; T-CELL; BLOCKADE;

D O I：

10.4049/jimmunol.1101737

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

071005 [微生物学]; 100108 [医学免疫学];

摘要：

IL-6 is a known downstream target of IL-1 beta and is consistently increased in serum from patients with NLRP3 inflammasome-mediated conditions. Therefore, IL-6 could be a therapeutic target in the treatment of IL-1 beta-provoked inflammation. IL-6 was increased in serum with accompanying neutrophilia in tissues of an inducible mouse model of Muckle-Wells syndrome. However, an IL-6-null background failed to provide phenotypic rescue and did not significantly impact inflammatory cytokine levels. In a second model of IL-1 beta-driven inflammation, NLRP3 activation by monosodium urate crystals similarly increased IL-6. Consistent with our Muckle-Wells syndrome model, ablation of IL-6 did not impact an acute neutrophilic response in this in vivo evaluation of gouty arthritis. Taken together, our results indicate that IL-6 is a reliable marker of inflammation, with no direct role in inflammasome-mediated disease. The Journal of Immunology, 2012, 189: 2707-2711.

引用

页码：2707 / 2711

页数：5

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