Circulating adiponectin levels in Indian patients with psoriasis and its relation to metabolic syndrome

Madanagobalane, Shraddha; Sandhya, V.; Anandan, Sambandam; Seshadri, Krishna G

doi:10.4103/2230-8210.129110

Cited by 8 publications

(2 citation statements)

References 27 publications

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“…Recent evidence highlights the important and potentially beneficial role of adiponectin in psoriasis. To begin with, patients with psoriasis have a significantly decreased level of adiponectin compared to healthy controls [ 122 , 123 ]. Secondly, the treatment of psoriasis leads to an elevation of the serum adiponectin level [ 124 ].…”

Section: Adiponectinmentioning

confidence: 99%

The Role of Adipokines in the Pathogenesis of Psoriasis

Kiełbowski

Bakinowska

Ostrowski

et al. 2023

IJMS

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Psoriasis is a chronic and immune-mediated skin condition characterized by pro-inflammatory cytokines and keratinocyte hyperproliferation. Dendritic cells, T lymphocytes, and keratinocytes represent the main cell subtypes involved in the pathogenesis of psoriasis, while the interleukin-23 (IL-23)/IL-17 pathway enhances the disease progression. Human adipose tissue is an endocrine organ, which secretes multiple proteins, known as adipokines, such as adiponectin, leptin, visfatin, or resistin. Current evidence highlights the immunomodulatory roles of adipokines, which may contribute to the progression or suppression of psoriasis. A better understanding of the complexity of psoriasis pathophysiology linked with adipokines could result in developing novel diagnostic or therapeutic strategies. This review aims to present the pathogenesis of psoriasis and the roles of adipokines in this process.

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Section: Adiponectinmentioning

confidence: 99%

The Role of Adipokines in the Pathogenesis of Psoriasis

Kiełbowski

Bakinowska

Ostrowski

et al. 2023

IJMS

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“…It can suppress the production of pro-inflammatory cytokines and promote the secretion of anti-inflammatory cytokines ( 14 , 15 ). Studies have shown that adiponectin levels are often decreased in patients with psoriasis ( 16 , 17 ). This reduction in adiponectin level is suggested to contribute to persistent inflammation; however, the mechanisms are not fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

Co-occurrence of non-alcoholic steatohepatitis exacerbates psoriasis associated with decreased adiponectin expression in a murine model

Takezaki,

Morizane,

Ikeda

et al. 2023

Front. Immunol.

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IntroductionClinical studies have suggested a bidirectional association between non-alcoholic steatohepatitis (NASH) and psoriasis, affecting each other’s development and severity. Here, we explored bidirectional causal linkages between NASH and psoriasis using a murine model.MethodsNASH was induced in mice by streptozotocin injection at 2 days of age and by high-fat diet feeding (STAM™ model). Psoriasis was induced by topical application of imiquimod (IMQ) on the ear. The severities of liver damage and psoriatic skin changes were determined using histological analysis. Gene expression in the skin tissues was evaluated using quantitative PCR analysis. Serum cytokine levels were determined using enzyme-linked immunosorbent assay. To examine the innate immune responses of normal human epidermal keratinocytes (NHEKs), the cells were treated with interleukin (IL)-17A, tumor necrosis factor (TNF)-α, and AdipoRon, an adiponectin receptor agonist.Results and DiscussionThere were no differences in the degree of liver tissue damage (fat deposition, inflammation, and fibrosis) between NASH mice with and those without psoriasis. Conversely, the co-occurrence of NASH significantly augmented psoriatic skin changes, represented by epidermal hyperplasia, in psoriatic mice. Pro-inflammatory cytokines were expressed in the inflamed skin of psoriatic mice, and the expression of genes, especially Il23a, Il1b, Il36g, and Mip2, was significantly upregulated by the co-occurrence of NASH. The expression of keratinocyte activation marker genes Defb4b and Krt16 was also upregulated by the co-occurrence of NASH. The serum TNF-α and IL-17 levels were increased by the co-occurrence of NASH and psoriasis. The serum adiponectin levels decreased in NASH mice compared with that in non-NASH mice. In NHEK culture, TNF-α and IL-17A synergistically upregulated CXCL1, CXCL8, and IL1B expression. The upregulated pro-inflammatory gene expression was suppressed by AdipoRon treatment, reflecting the anti-inflammatory capacity of adiponectin.ConclusionThe co-occurrence of NASH exacerbated psoriatic skin changes associated with increased serum inflammatory cytokine levels and decreased serum adiponectin levels. Combined with in vitro findings, increased inflammatory cytokine levels and decreased adiponectin levels likely promote innate immune responses in epidermal keratinocytes in psoriatic skin lesions. Overall, therapeutic intervention for co-occurring NASH is essential to achieve a favorable prognosis of psoriasis in clinical practice.

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