Leptin is associated with disease activity but not with anthropometric indices in rheumatoid arthritis patients

Dervišević, Amela; Resić, Halima; Sokolović, Šekib; Babić, Nermina; Avdagić, Nesina; Začiragić, Asija; Bećiragić, Amela; Fajkić, Almir; Lepara, Orhan; Hadžović-Dzuvo, Almira

doi:10.5114/aoms.2017.65080

Cited by 13 publications

(14 citation statements)

References 32 publications

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“…As previously described, we also found a relation between BMI and leptin levels [21,35]. In some studies on rheumatoid arthritis, leptin was correlated with disease activity, although it was not associated with BMI [38,39]. This dissociation may be related to the fact that leptin synthesis does not occur in only abdominal fat.…”

Section: Discussionsupporting

confidence: 73%

Comparisons of Comorbidities in Patients with Ankylosing Spondylitis and Psoriatic Arthritis and their Influence on Psoriatic Arthritis Disease Activity: Results of a Multicentre Longitudinal Study

Montilla

Acosta

Gómez-Lechón

et al. 2021

Preprint

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Objectives: To compare the presence of psycho-affective disorders and obesity-associated factors between ankylosing spondylitis (AS) and psoriatic arthritis (PsA) patients and to corelate these comorbidities with PsA disease activity.Methods: This prospective observational longitudinal study included 216 PsA patients and 114 AS patients. Anxiety and depression were compared between both patient groups using the Hospital Anxiety and Depression Scale (HADS) questionnaire. We compared the waist/hip ratio, body mass index (BMI) and laboratory variables including apolipoprotein A, apolipoprotein B, lipoprotein A, the ApoB/ApoA ratio, peptide C, insulin, resistance to insulin (HOMA-IR) and leptin. PsA activity was evaluated by the Disease Activity Index for Psoriatic Arthritis (DAPSA) score every 4 months for a year. Patients were divided into two groups: those with moderate or high activity and those with low activity or remission. We compared anxiety-, depression- and obesity-related factors between these two groups.Results: There were no differences in baseline characteristics between AS and PsA patients. Among the studied factors, only serum leptin was significantly higher in PsA patients than in AS patients (18.49±19.01 vs 11.5±10.05, p<0.01). Initial serum leptin, obesity and depressive behaviour were poor prognostic factors for persistent low disease activity. The leptin level was correlated with the visual analogue scale (VAS) pain score (R=0.21, p<0.01), VAS activity score (R=0.26, p<0.01), swollen joint count (SJC) (R=0.23, p<0.01) and tender joint count (TJC) (R=0.26, p<0.01).Conclusion: Obesity alone or concurrent with increased leptin secretion and depression may influence persistent PsA activity. Leptin levels differentiated PsA patients from AS patients.

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Section: Discussionsupporting

confidence: 73%

Comparisons of Comorbidities in Patients with Ankylosing Spondylitis and Psoriatic Arthritis and their Influence on Psoriatic Arthritis Disease Activity: Results of a Multicentre Longitudinal Study

Montilla

Acosta

Gómez-Lechón

et al. 2021

Preprint

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“…We also assessed the influence of IFN-γ and TNF on leptin recepter (ObR) expression and found this combination to increase ObR surface levels. Like IFN-γR, ObR signaling is initiated by JAK/STAT activation and some effects of IFN-γ are potentiated by leptin which has been associated with disease activity in RA 18,33 . In addition, TNF has been shown to increase surface levels of ObR by the activation of protein kinase C 34 .…”

Section: Discussionmentioning

confidence: 99%

Positive and negative cooperativity of TNF and Interferon-γ in regulating synovial fibroblast function and B cell survival in fibroblast/B cell co-cultures

Lowin

Anssar

Bäuml

et al. 2020

Sci Rep

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Synovial fibroblasts (SF) were reported to produce B cell activating factor (BAFF) in response to stimulation with interferon-γ (IFN-γ) or tumor necrosis factor (TNF). However, the influence of these pro-inflammatory cytokines on other receptors/ligands of the TNF superfamily or associated cytokine receptors in SF has not been investigated yet. Here we show the differential regulation of BAFF (CD257), Fn14 (CD266), TACI (CD267), BAFF-R (CD268), BCMA (CD269), CD40 ligand (CD40L, CD154), IFN-γR (CD119), Leptin receptor (ObR, CD295), VCAM-1 (CD106) and membrane TGF-β in isolated Sf and the impact of ifn-γ/TNF co-incubation on proliferation, IL-6 and IL-8 production. In addition, the impact of differentially stimulated SF on B cell survival in co-cultures was assessed. Surface cytokines and cytokine receptors were detected by flow cytometry. Soluble cytokine receptors and cytokines were quantified by ELISA. Proliferation was assessed by cell titer blue. Murine B cell survival in fibroblast/ B cell co-cultures was determined by annexin V/propidium iodide staining and flow cytometry. IFN-γ together with TNF synergistically and significantly increased the cell surface levels of BAFF, Fn14, TACI, BAFF-R, BCMA, CD40L, ObR and IFN-γR in rheumatoid arthritis SF after 72 h incubation. Soluble BAFF was only induced by IFN-γ and inhibited by TNF. Addition of TWEAK had no influence on proliferation or IL-8 production but decreased TNF-induced IL-6 production, whereas APRIL, BAFF and leptin did not modulate TNF or TNF/IFN-γ-induced proliferation or cytokine production. Proliferation was increased by TNF and further enhanced by the addition of IFN-γ. In co-culture experiments, SF stimulated with TNF/IFN but not TNF or IFN-γ alone increased shedding of VCAM-1 and expression of membrane TGFβ, which was associated with reduced survival of murine B cells. ifn-γ and TNF regulate the expression of TNF family member cytokines and associated receptors. Ligation of IFN-γR and Fn14 under proinflammatory conditions modulated IL-6/IL-8 production and proliferation. In B cell/SF co-cultures, the combination of TNF/IFN reduced B cell survival possibly via enhanced VCAM-1 shedding and/ or increased tGf-β production. ifn-γ is necessary for the observed effects on B cell survival and SF cytokine production and emphasizes its anti-inflammatory role in rheumatoid arthritis. In rheumatoid arthritis (RA), interferon-γ (IFN-γ) levels are increased in synovial fluid and concomitantly, synovial fluid mononuclear cells show increased IFN-γ mRNA levels 1,2. IFN-γ has a dual role in chronic inflammation since it does increase the presentation of antigens via induction of MHC class II molecules in synovial fibroblasts

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“…Leptin binds to its receptors on neutrophils 105 and activates the chemotaxis and phagocytosis process. 106 The effect of leptin on the generation of reactive oxygen species is still undefined, 105 but it causes the migration of leukocytes toward injured tissue. 106 At the onset of inflammation, leptin increases the synthesis of pro-inflammatory mediators like IL-6 and TNF-α.…”

Section: Leptin Involved In the Progression Of Atherosclerosis In Type II Diabetes Mellitusmentioning

confidence: 99%

Effect of Leptin on Chronic Inflammatory Disorders: Insights to Therapeutic Target to Prevent Further Cardiovascular Complication

Dessie¹,

Ayelign²,

Akalu³

et al. 2021

DMSO

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In response to obesity-associated chronic inflammatory disorders, adipose tissue releases a biologically active peptide known as leptin. Leptin activates the secretion of chemical mediators, which contribute to the pathogenesis of chronic inflammatory disorders, such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and psoriasis. Conversely, adiposity and obesity are the major aggravating risk factors in the pathogenesis of metabolic syndrome (MetS), including type II diabetes mellitus and obesity-associated hypertension. Elevated level of leptin in obesity-associated hypertension causes an increase in the production of aldosterone, which also results in elevation of arterial blood pressure. Hyperleptinemia is associated with the progress of the atherosclerosis through secretion of pro-inflammatory cytokines, like interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), IL-17, and other cytokines to promote inflammation. The release of those cytokines leads to chronic inflammatory disorders and obesity-associated MetS. Thus, the aberrant leptin level in both MetS and chronic inflammatory disorders also leads to the complication of cardiovascular diseases (CVD). Therapeutic target of leptin regarding its pro-inflammatory effect and dysregulated sympathetic nervous system activity may prevent further cardiovascular complication. This review mainly assesses the mechanism of leptin on the pathogenesis and further cardiovascular risk complication of chronic inflammatory disorders.

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Leptin is associated with disease activity but not with anthropometric indices in rheumatoid arthritis patients

Cited by 13 publications

References 32 publications

Comparisons of Comorbidities in Patients with Ankylosing Spondylitis and Psoriatic Arthritis and their Influence on Psoriatic Arthritis Disease Activity: Results of a Multicentre Longitudinal Study

Comparisons of Comorbidities in Patients with Ankylosing Spondylitis and Psoriatic Arthritis and their Influence on Psoriatic Arthritis Disease Activity: Results of a Multicentre Longitudinal Study

Positive and negative cooperativity of TNF and Interferon-γ in regulating synovial fibroblast function and B cell survival in fibroblast/B cell co-cultures

Effect of Leptin on Chronic Inflammatory Disorders: Insights to Therapeutic Target to Prevent Further Cardiovascular Complication

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