Adiponectin differentially regulates cytokines in porcine macrophages

Wulster-Radcliffe, Meghan; Ajuwon, Kolapo M.; Wang, Jiazhen; Christian, John A.; Spurlock, Michael E.

doi:10.1016/j.bbrc.2004.02.130

Cited by 412 publications

(300 citation statements)

References 21 publications

Supporting

Mentioning

278

Contrasting

Unclassified

Order By: Relevance

“…Therefore, adiponectin probably exerts its hepatoprotective effects in the model of acute liver inflammation induced by ConA by a mechanism independent of TNF-a down-regulation. We and others recently described an anti-inflammatory role of adiponectin on in vitro cultured myeloid cells [3,4,7]. Pre-treatment of monocytes and monocyte-derived cells (i.e.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Up-regulation of the anti-inflammatory adipokine adiponectin in acute liver failure in mice

Wolf¹,

Wolf²,

Avila³

et al. 2006

Journal of Hepatology

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

“…We and others recently demonstrated potent antiinflammatory properties of adiponectin [3,4]. Apart from downregulation of the synthesis of the pro-inflammatory cytokine TNF-a, adiponectin leads to an increased production of the anti-inflammatory mediators IL-10 and IL-1RA in human myeloid cells [3].…”

Section: Introductionmentioning

confidence: 94%

Up-regulation of the anti-inflammatory adipokine adiponectin in acute liver failure in mice

Wolf¹,

Wolf²,

Avila³

et al. 2006

Journal of Hepatology

View full text Add to dashboard Cite

“…It is produced mainly in WAT and also in bone marrow, the spleen, lungs, placentas and the pancreas. Resistin takes part in adipogenesis, insulin resistance and inflammatory processes and exhibits a positive correlation with the occurrence of obesity, insulin resistance, and chronic inflammation [33]. It induces the secretion of pro-inflammatory cytokines such as IL-1, IL-6, IL-12 and TNF-α in a NF-κB-mediated fashion [34,35].…”

Section: Resistinmentioning

confidence: 99%

The role of adipocytokines in the pathogenesis of knee joint osteoarthritis

Richter

Trzeciak

Owecki

et al. 2015

International Orthopaedics (SICOT)

View full text Add to dashboard Cite

Osteoarthritis (OA) is one of the most common causes of musculoskeletal disability in the world. Traditionally, it has been thought that obesity contributes to the development and progression of OA by increased mechanical load of the joint structures. Nevertheless, studies have shown that adipose tissue-derived cytokines (adipocytokines) are a possible link between obesity and OA. Furthermore, according to recent findings, not only articular cartilage may be the main target of these cytokines but also the synovial membrane, subchondral bone and infrapatellar fat pad may be encompassed in the process of degradation. This review presents the most recent reports on the contribution of adipocytokines to the knee joint cartilage degradation, osteophyte formation, infrapatellar fat pad alterations and synovitis.

show abstract

“…In vitro models have suggested that the immunomodulatory actions of adiponectin are anti-inflammatory [8][9][10][11][12][13][14], as exemplified by its in vitro ability to attenuate lipopolysaccharide (LPS) induction of tumour necrosis factor (TNF-a) [8,14,15].…”

Section: Introductionmentioning

confidence: 99%

Induction of TLR Tolerance in Human Macrophages by Adiponectin: Does LPS Play a Role?

et al. 2009

View full text Add to dashboard Cite

Obesity is regarded as a pro‐inflammatory state. It is associated with low circulating levels of the adipokine, adiponectin, which is considered to be an anti‐inflammatory. However, adiponectin knockout mice do not consistently demonstrate pro‐inflammatory phenotypes, suggesting more complexity in the in vivo immunomodulatory effects of adiponectin than originally anticipated. Moreover, adiponectin exerts pro‐inflammatory effects in some experimental systems. This contradiction has been resolved by hypothesizing that adiponectin induces tolerance to inflammatory stimuli, notably Toll‐like receptor (TLR) ligands. We noticed that this effect resembled lipopolysaccharide (LPS) tolerance and therefore tested adiponectin from a variety of sources for LPS contamination. All adiponectin tested carried low levels of LPS in the range of 1–30 pg/μg of adiponectin, sufficient to produce final LPS concentrations in the pg/ml range under experimental conditions. We found that induction of tolerance to TLR ligands by adiponectin in human monocyte‐derived macrophages could be reproduced by such LPS concentrations. Moreover, the LPS antagonist, polymixin B, substantially inhibited induction of tolerance by adiponectin. Furthermore, polymixin B and a naturally occurring antagonist LPS were able to partially attenuate induction of tumour necrosis factor‐α and interleukin‐6 in human monocyte‐derived macrophages by adiponectin. Polymixin B also inhibited nuclear factor‐κB and mitogen‐activated protein kinase signalling elicited by adiponectin. We therefore propose that some of adiponectin’s immunomodulatory effects, in particular, its TLR‐tolerising actions in human monocyte‐derived macrophages, may be confounded by induction of tolerance by contaminating LPS.

show abstract

Adiponectin differentially regulates cytokines in porcine macrophages

Cited by 412 publications

References 21 publications

Up-regulation of the anti-inflammatory adipokine adiponectin in acute liver failure in mice

Up-regulation of the anti-inflammatory adipokine adiponectin in acute liver failure in mice

The role of adipocytokines in the pathogenesis of knee joint osteoarthritis

Induction of TLR Tolerance in Human Macrophages by Adiponectin: Does LPS Play a Role?

Contact Info

Product

Resources

About