Increased activity of interleukin-23/interleukin-17 proinflammatory axis in obese women

Šumarac-Dumanović, Mirjana; Stevanović, Darko; Ljubic, A; Jorga, Jagoda; Simić, Miloš; Stamenkovic-Pejkovic, Danica; Starčević, Vesna; Trajkovič, Vladimir; Micić, Dragan

doi:10.1038/ijo.2008.216

Cited by 250 publications

(214 citation statements)

References 39 publications

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“…DIO is reversible and it should be interesting to assess, to what extent and at which disease stage weight loss can reduce Th17 expansion and disease exacerbation, information that might have clinical impact. While this present manuscript was in submission, first observations from a small clinical study demonstrated elevated IL-17 serum levels in obese patients [21], suggesting that our observations in rodents are likely relevant to human disease. IL-6-dependent Th17 expansion is a clinically prominent element of pro-inflammatory diseases in obesity.…”

Section: Discussionmentioning

confidence: 72%

Obesity predisposes to Th17 bias

et al. 2009

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Obesity is associated with numerous inflammatory conditions including atherosclerosis, autoimmune disease and cancer. Although the precise mechanisms are unknown, obesity‐associated rises in TNF‐α, IL‐6 and TGF‐β are believed to contribute. Here we demonstrate that obesity selectively promotes an expansion of the Th17 T‐cell sublineage, a subset with prominent pro‐inflammatory roles. T‐cells from diet‐induced obese mice expand Th17 cell pools and produce progressively more IL‐17 than lean littermates in an IL‐6‐dependent process. The increased Th17 bias was associated with more pronounced autoimmune disease as confirmed in two disease models, EAE and trinitrobenzene sulfonic acid colitis. In both, diet‐induced obese mice developed more severe early disease and histopathology with increased IL‐17+ T‐cell pools in target tissues. The well‐described association of obesity with inflammatory and autoimmune disease is mechanistically linked to a Th17 bias.

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Section: Discussionmentioning

confidence: 72%

Obesity predisposes to Th17 bias

et al. 2009

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“…Recently, besides the classic proinflammatory cytokine TNF-a, the role of IL-17 in adipose tissue and fat metabolism has been drawing attention 53,54 . Clinical studies have demonstrated that obese women exhibit increased levels of circulating IL-23 and IL-17, suggesting a potential role for IL-17 in obesity 55 . As comparable to human studies, several animal experiments indicate that obesity promotes Th17 expansion and subsequent IL-17 production, exacerbating disease severity in murine models of multiple sclerosis and inflammatory bowel disease, both of which are representative Th17-related diseases as well as psoriasis 56 .…”

Section: Discussionmentioning

confidence: 99%

Adiponectin regulates psoriasiform skin inflammation by suppressing IL-17 production from γδ-T cells

et al. 2015

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Accumulating epidemiologic evidence has revealed that metabolic syndrome is an independent risk factor for psoriasis development and is associated with more severe psoriasis. Adiponectin, primarily recognized as a metabolic mediator of insulin sensitivity, has been newly drawing attention as a mediator of immune responses. Here we demonstrate that adiponectin regulates skin inflammation, especially IL-17-related psoriasiform dermatitis. Mice with adiponectin deficiency show severe psoriasiform skin inflammation with enhanced infiltration of IL-17-producing dermal Vg4 þ gd-T cells. Adiponectin directly acts on murine dermal gd-T cells to suppress IL-17 synthesis via AdipoR1. We furthermore demonstrate here that the adiponectin level of skin tissue as well as subcutaneous fat is decreased in psoriasis patients. IL-17 production from human CD4-or CD8-positive T cells is also suppressed by adiponectin. Our data provide a regulatory role of adiponectin in skin inflammation, which would imply a mechanism underlying the relationship between psoriasis and metabolic disorders.

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“…In addition, decreased blood level of adiponectin in obesity also contributes to the action of the pathway as adiponectin can block insulin and leptin [Fujisawa et al, 2008;Huang and Chen, 2009a]. Recently, IL23/17 has also been shown to be activated in obesity which in turn activates the Src/PI3K/Akt pathway [Hsieh et al, 2002;Sumarac-Dumanovic et al, 2009].…”

Section: Activation Of the Src/pi3k/akt Signal Pathway In Obesitymentioning

confidence: 99%

The Src/PI3K/Akt signal pathway may play a key role in decreased drug efficacy in obesity‐associated cancer

Chen¹

2010

J of Cellular Biochemistry

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Increased activity of interleukin-23/interleukin-17 proinflammatory axis in obese women

Cited by 250 publications

References 39 publications

Obesity predisposes to Th17 bias

Obesity predisposes to Th17 bias

Adiponectin regulates psoriasiform skin inflammation by suppressing IL-17 production from γδ-T cells

The Src/PI3K/Akt signal pathway may play a key role in decreased drug efficacy in obesity‐associated cancer

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