Affective temperament, depressive symptoms
and interleukins in patients with psoriasis

Marek-Józefowicz, Luiza; Jaracz, Marcin; Borkowska, Alina

doi:10.5114/ada.2021.104289

Cited by 6 publications

(8 citation statements)

References 42 publications

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“…Differently, Marek-Józefowicz et al. [ 61 ] identified as a shared biological mechanism the increased IL-6 plasma levels in a cohort of Ps patients with comorbid depression and specific affective temperament dimensions ( Table 3 ).…”

Section: Resultsmentioning

confidence: 99%

“…In addition, Griffiths et al [ 41 ] reported the efficacy of such biologic on depression and serum levels of sCRP, suggesting that both systemic inflammatory markers and IL-17A may be involved in Ps comorbid depressive patients. Differently, Marek-Józefowicz et al [ 61 ] reported the increased plasma concentrations of IL-6 as a shared biological mechanism in Ps depressed patients with specific affective temperament dimensions.…”

Section: Discussionmentioning

confidence: 99%

“…The authors reported as common biological markers high concentrations of interleukin 18 (IL-18) and low concentrations of 25-hydroxyvitamin D 3 (25-hydroxy-vit D 3 ) associated with depression severity in men with Ps and high body mass index (BMI). Differently, Marek-Józefowicz et al [61] identified as a shared biological mechanism the increased IL-6 plasma levels in a cohort of Ps patients with comorbid depression and specific affective temperament dimensions (Table 3).…”

Section: Clinical Studiesmentioning

confidence: 99%

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A systematic review on shared biological mechanisms of depression and anxiety in comorbidity with psoriasis, atopic dermatitis, and hidradenitis suppurativa

et al. 2021

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Background Mental disorders in comorbidity with chronic skin diseases may worsen disease outcome and patients’ quality of life. We hypothesized the comorbidity of depression, anxiety syndromes, or symptoms as attributable to biological mechanisms that the combined diseases share. Methods We conducted a systematic review based on the Preferred Reporting Items for Systematic Review and Meta-Analysis statement searching into PubMed, PsycInfo, and Scopus databases. We examined the literature regarding the comorbidity of psoriasis (Ps), atopic dermatitis (AD), or hidradenitis suppurativa with depression and/or anxiety in adults ≥18 years and the hypothetical shared underlying biological mechanisms. Results Sixteen studies were analyzed, mostly regarding Ps and AD. Brain-derived neurotrophic factor/tropomyosin receptor kinase B signaling and nuclear factor kappa-light-chain-enhancer of activated B cells/p38 mitogen-activated protein kinase pathways arose as shared mechanisms in Ps animal models with depression- and/or anxiety-like behaviors. Activated microglia and neuroinflammatory responses emerged in AD depressive models. As to genetic studies, atopic-dermatitis patients with comorbid anxiety traits carried the short variant of serotonin transporter and a polymorphism of the human translocator protein gene. A GA genotype of catechol-O-methyltransferase gene was instead associated with Ps. Reduced natural killer cell activity, IL-4, serotonin serum levels, and increased plasma cortisol and IgE levels were hypothesized in comorbid depressive AD patients. In Ps patients with comorbid depression, high serum concentrations of IL-6 and IL-18, as well as IL-17A, were presumed to act as shared inflammatory mechanisms. Conclusions Further studies should investigate mental disorders and chronic skin diseases concurrently across patients’ life course and identify their temporal relation and biological correlates. Future research should also identify biological characteristics of individuals at high risk of the comorbid disorders and associated complications.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Clinical Studiesmentioning

confidence: 99%

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A systematic review on shared biological mechanisms of depression and anxiety in comorbidity with psoriasis, atopic dermatitis, and hidradenitis suppurativa

et al. 2021

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“…The role of IL6 in psoriasis comorbidities (e.g., depression) has been established [ 55 , 56 ], whereas its involvement in atopic dermatitis comorbidities is far from being proven, although data from literature seem to indicate that the prevalence of depression among atopic patients is higher than in the general population [ 57 ], and the role of IL6 need to be investigated in more detail. In this regard, in 2020, He et al emphasized the potential utility of tape-strip proteomic profiling for tracking biomarkers of therapeutic response in real-life settings, as well as clinical trials and longitudinal studies of AD [ 48 ].…”

Section: Discussionmentioning

confidence: 99%

Mesenchymal Stem Cells Profile in Adult Atopic Dermatitis and Effect of IL4-IL13 Inflammatory Pathway Inhibition In Vivo: Prospective Case-Control Study

Campanati

Orciani

Marani

et al. 2022

JCM

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Atopic dermatitis (AD) is an inflammatory disease that typically begins in childhood and may persist into adulthood, becoming a lifelong condition. The major inflammatory mediators of AD are known to be interleukin IL4 and IL13, so Dupilumab, which is able to inhibit both interleukins by blocking the shared IL4Rα subunit, has become an attractive option for treating AD. Mesenchymal stem cells (MSCs) are involved in the onset and development of AD by secreting specific interleukins. The aim of this study was to isolate MSCs from healthy controls (C-MSCs) and patients with AD before (AD-MSCs T0) and after 16 weeks of treatment with Dupilumab (AD-MSCs T16); to evaluate the expression mainly of IL4 and IL13 and of other inflammatory cytokines in C-MSCs, AD-MSCs at T0 and at T16; and to evaluate the efficacy of Dupilumab on MSCs immunobiology. C- and AD-MSCs (T0, T16) were isolated from skin specimens and characterized; the expression/secretion of IL4 and IL13 was evaluated using immuno-cytochemistry (ICC), indirect immune-fluorescence (IIF) and an ELISA test; secretion of IL2, IL4, IL5, IL6, IL10, IL12, IL13, IL17A, Interferon gamma (IFNγ), Tumor necrosis factor alpha (TNFα), Granulocyte Colony-Stimulating Factor (G-CSF), and Transforming Growth Factor beta1 (TGFβ1) were measured with ELISA. IL13 and IL6 were over-expressed, while IL4 was down-regulated in AD-MSCs at T0 compared to C-MSCs. IL6 and IL13 expression was restored after 16 weeks of Dupilumab treatment, while no significant effects on IL4 expression were noted. Finally, IL2, IL5, IL10, IL12, IL17A, INFγ, TNFα, G-CSF, and TGFβ1 were similarly secreted by C- and AD-MSCs. Although Dupilumab blocks the IL4Rα subunit shared by IL4 and IL13, it is evident that its real target is IL13, and its ability to target IL13 in MSCs reinforces the evidence, already known in differentiated cells, of the central role IL13 rather than IL4 in the development of AD. The inflammatory cascade in AD begins at the mesenchymal level, so an upstream therapeutic intervention, able to modify the immunobiology of atopic MSCs, could potentially change the natural history of the disease.

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“…[45][46][47][48][49] IL-6 also predisposes patients with psoriasis to more frequent occurrences of depressive episodes, lipid abnormalities and cardiovascular comorbidities. [50][51][52] Imiquimod increases the production of IL-6 in the adipose tissue of obese mice and higher IL-6 levels increase Th17 cell differentiation compared with those in normal mice. 53 Cutaneous IL-6-siRNA targeting using ablative lasers to deliver the nanocarriers effectively attenuates psoriasiform dermatitis.…”

Section: Discussionmentioning

confidence: 99%

Serine deficiency exacerbates psoriatic skin inflammation by regulating S‐adenosyl methionine‐dependent DNA methylation and NF‐κB signalling activation in keratinocytes

Meng,

Liu,

Yao

et al. 2023

Acad Dermatol Venereol

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BackgroundSerine metabolism is crucial for tumor oncogenesis and immune responses. S‐adenosyl methionine (SAM), a methyl donor, is typically derived from serine‐driven one‐carbon metabolism. However, the involvement of serine metabolism in psoriatic skin inflammation remains unclear.ObjectivesTo investigate the association between serine metabolism and psoriatic skin inflammation.MethodsClinical samples were collected from patients with psoriasis and the expression of serine biosynthesis enzymes was evaluated. The HaCaT human keratinocyte cell line was transfected with small interfering RNA (siRNA) of key enzyme or treated with inhibitors. RNA sequencing and DNA methylation assays were performed to elucidate the mechanisms underlying serine metabolism‐regulated psoriatic keratinocyte inflammation An imiquimod (IMQ)‐induced psoriasis mouse model was established to determine the effect of the SAM administration on psoriatic skin inflammation.ResultsThe expression of serine synthesis pathway enzymes, including the first rate‐limiting enzyme in serine biosynthesis, phosphoglycerate dehydrogenase (PHGDH), was downregulated in the epidermal lesions of patients with psoriasis compared with that in healthy controls. Suppressing PHGDH in keratinocytes promoted the production of proinflammatory cytokines and enrichment of psoriatic‐related signaling pathways, including the tumor necrosis factor‐alpha (TNF‐α) signaling pathway, interleukin (IL)‐17 signaling pathway, and NF‐κB signaling pathway. In particular, PHGDH inhibition markedly promoted the secretion of IL‐6 in keratinocytes with or without IL‐17A, IL‐22, IL‐1α, oncostatin M, and TNF‐α (mix) stimulation. Mechanistically, PHGDH inhibition upregulated the expression of IL‐6 by inhibiting SAM‐dependent DNA methylation at the promoter and increasing the binding of myocyte enhancer factor 2A. Furthermore, PHGDH inhibition increased the secretion of IL‐6 by increasing the activation of NF‐κB via SAM inhibition. SAM treatment effectively alleviated IMQ‐induced psoriasis‐like skin inflammation in mice.ConclusionsOur study revealed the crucial role of PHGDH in antagonizing psoriatic skin inflammation and indicated that targeting serine metabolism may represent a novel therapeutic strategy for treating psoriasis.

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Affective temperament, depressive symptoms and interleukins in patients with psoriasis

Cited by 6 publications

References 42 publications

A systematic review on shared biological mechanisms of depression and anxiety in comorbidity with psoriasis, atopic dermatitis, and hidradenitis suppurativa

A systematic review on shared biological mechanisms of depression and anxiety in comorbidity with psoriasis, atopic dermatitis, and hidradenitis suppurativa

Mesenchymal Stem Cells Profile in Adult Atopic Dermatitis and Effect of IL4-IL13 Inflammatory Pathway Inhibition In Vivo: Prospective Case-Control Study

Serine deficiency exacerbates psoriatic skin inflammation by regulating S‐adenosyl methionine‐dependent DNA methylation and NF‐κB signalling activation in keratinocytes

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