Adiponectin Promotes Macrophage Polarization toward an Anti-inflammatory Phenotype*

By K. Ohashi, J. Parker, N. Ouchi, A. Higuchi, J. Vita, N. Gokce, A. A. Pedersen, Christoph Kalthoff, Søren Tullin, A. Sams and 2 more. Journal of Biological Chemistry, 2009

626 citations recorded by the source corpus.

It is established that the adipocyte-derived cytokine adiponectin protects against cardiovascular and metabolic diseases, but the effect of this adipokine on macrophage polarization, an important mediator of disease progression, has never been assessed. We hypothesized that adiponectin modulates macrophage polarization from that resembling a classically activated M1 phenotype to that resembling alternatively-activated M2 cells. Peritoneal macrophages and the stromal vascular fraction (SVF) cells of adipose tissue isolated from adiponectin knock-out mice displayed increased M1 markers, including tumor necrosis factor-α, interleukin-6, and monocyte chemoattractant protein-1 and decreased M2 markers, including arginase-1, macrophage galactose N-acetyl-galactosamine specific lectin-1, and interleukin-10. The systemic delivery of adenovirus expressing adiponectin significantly augmented arginase-1 expression in peritoneal macrophages and SVF cells in both wild-type and adiponectin knock-out mice. In culture, the treatment of macrophages with recombinant adiponectin protein led to an increase in the levels of M2 markers and a reduction of reactive oxygen species and reactive oxygen species-related gene expression. Adiponectin also stimulated the expression of M2 markers and attenuated the expression of M1 markers in human monocyte-derived macrophages and SVF cells isolated from human adipose tissue. These data show that adiponectin functions as a regulator of macrophage polarization, and they indicate that conditions of high adiponectin expression may deter metabolic and cardiovascular disease progression by favoring an anti-inflammatory phenotype in macrophages.

Subfields: Epidemiology, Immunology

View Paper: https://www.semanticscholar.org/paper/3a59d60437fbca8af209ec2ee185b365d426d877

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In Epidemiology

1. H. Fang
2. R. L. Judd
3. Herbert Tilg
4. A. Moschen
5. K. Walsh
6. P. Scherer
7. P. Seale
8. N. Ouchi

In Immunology

1. H. Fang
2. R. L. Judd
3. P. Scherer

Citations in the corpus

• Adiponectin Regulation and Function (2018, positive): “Adiponectin regulates macrophage polarization, shifting the polarization state from the proinflammatory M1 state to an anti-inflammatory M2 state (79, 223).”
• Adipokines in inflammation and metabolic disease (2011, background): “Peritoneal macrophages and adipose tissue stromal vascular fraction cells of adiponectin-deficient mice show increased expression of pro-inflammatory M1-type markers and decreased expression of anti-inflammatory M2-type marker”
• Adipose tissue plasticity in health and disease (2022, background): “By contrast, adiponectin promotes an anti-inflammatory profile in macrophages (Ohashi et al., 2010).”
• Adiponectin: mechanistic insights and clinical implications (2012, background): “Peritoneal [60], alveolar [60] and hepatic macrophages [65] all display M2 polarisation under the influence of adiponectin.”
• Evolution of inflammation in nonalcoholic fatty liver disease: The multiple parallel hits hypothesis (2010, background): “Importantly, adiponectin and PPARc promote adipose tissue macrophage polarization toward an alternative/anti-inflammatory phenotype.(78,79) Altogether, our and several other studies(80) present evidence that adipose tissue inflammation is a common event in morbid obesity, and this tissue could refle”
• New insights into oxidative stress and inflammation during diabetes mellitus-accelerated atherosclerosis (2018, background): “It promotes AMPK-dependent polarization of macrophages toward an anti-inflammatory phenotype [118], and can increase macrophage IL-6 via activation of NF-κB through AdipoRX (Fig.”
• GENeration (2015, neutral): “Once the "front-end" concept was working, the remaining conversion effort, to get all of NASTRAN on a "4G" computer, while involving significant volumes of code, would not require the further system type extensions.”