Adipose Tissue Macrophages Promote Myelopoiesis and Monocytosis in Obesity

被引：375

作者：

Nagareddy, Prabhakara R. ^{[1
,2
]}

Kraakman, Michael ^{[3
]}

Masters, Seth L. ^{[4
]}

Stirzaker, Roslynn A. ^{[1
]}

Gorman, Darren J. ^{[5
]}

Grant, Ryan W. ^{[6
]}

Dragoljevic, Dragana ^{[3
]}

Hong, Eun Shil ^{[7
]}

Abdel-Latif, Ahmed ^{[2
]}

Smyth, Susan S. ^{[2
]}

Choi, Sung Hee ^{[7
]}

Korner, Judith ^{[8
]}

Bornfeldt, Karin E. ^{[9
,10
]}

Fisher, Edward A. ^{[11
]}

Dixit, Vishwa Deep ^{[6
,12
]}

Tall, Alan R. ^{[5
]}

Goldberg, Ira J. ^{[1
,13
]}

Murphy, Andrew J. ^{[3
,5
,14
]}

机构：

[1] Columbia Univ, Dept Med, Div Prevent Med & Nutr, New York, NY 10032 USA

[2] Univ Kentucky, Dept Internal Med, Lexington, KY 40514 USA

[3] Baker IDI Heart & Diabet Inst, Melbourne, Vic 3004, Australia

[4] Walter & Eliza Hall Inst Med Res, Div Inflammat, Melbourne, Vic 3052, Australia

[5] Columbia Univ, Dept Med, Div Mol Med, New York, NY 10032 USA

[6] Louisiana State Univ, Pennington Biomed Res Inst, Baton Rouge, LA 70803 USA

[7] Seoul Natl Univ, Dept Med, Seoul 151742, South Korea

[8] Columbia Univ, Dept Med, Div Endocrinol, New York, NY 10032 USA

[9] Univ Washington, Dept Med, Seattle, WA 98109 USA

[10] Univ Washington, Dept Pathol, Seattle, WA 98109 USA

[11] NYU, Sch Med, Div Cardiol, New York, NY 10016 USA

[12] Yale Univ, Sch Med, Dept Immunobiol, New Haven, CT 06520 USA

[13] NYU, Sch Med, Div Endocrinol Diabet & Metab, New York, NY 10016 USA

[14] Monash Univ, Dept Immunol, Melbourne, Vic 3004, Australia

来源：

CELL METABOLISM | 2014年 / 19卷 / 05期

基金：

加拿大健康研究院; 英国医学研究理事会;

关键词：

STEM-CELL PROLIFERATION; NORMALIZES INSULIN SENSITIVITY; CORONARY-HEART-DISEASE; INTERLEUKIN-1-RECEPTOR ANTAGONIST; ATHEROSCLEROTIC PLAQUES; INDUCED INFLAMMATION; LOCAL PROLIFERATION; DIABETES-MELLITUS; NATIONAL SAMPLE; LEUKOCYTE COUNT;

D O I：

10.1016/j.cmet.2014.03.029

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Obesity is associated with infiltration of macrophages into adipose tissue (AT), contributing to insulin resistance and diabetes. However, relatively little is known regarding the origin of AT macrophages (ATMs). We discovered that murine models of obesity have prominent monocytosis and neutrophilia, associated with proliferation and expansion of bone marrow (BM) myeloid progenitors. AT transplantation conferred myeloid progenitor proliferation in lean recipients, while weight loss in both mice and humans (via gastric bypass) was associated with a reversal of monocytosis and neutrophilia. Adipose S100A8/A9 induced ATM TLR4/MyD88 and NLRP3 inflammasome-dependent IL-1 beta production. IL-1 beta interacted with the IL-1 receptor on BM myeloid progenitors to stimulate the production of monocytes and neutrophils. These studies uncover a positive feedback loop between ATMs and BM myeloid progenitors and suggest that inhibition of TLR4 ligands or the NLRP3-IL-1 beta signaling axis could reduce AT inflammation and insulin resistance in obesity.

引用

页码：821 / 835

页数：15

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