scholarly journals Increased Serum Interleukin-9 Levels in Rheumatoid Arthritis and Systemic Lupus Erythematosus: Pathogenic Role or Just an Epiphenomenon?

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Andréa Tavares Dantas ◽  
Claudia Diniz Lopes Marques ◽  
Laurindo Ferreira da Rocha Junior ◽  
Mariana Brayner Cavalcanti ◽  
Sayonara Maria Calado Gonçalves ◽  
...  
Keyword(s):  
Lupus Erythematosus ◽  
Disease Duration ◽  
Serum Levels ◽  
Significant Negative Correlation ◽  
Pathogenic Role ◽  
Laboratory Parameters ◽  
Interleukin 9 ◽  
Precise Role ◽  
Potential Use

The purpose of this paper was to evaluate the levels of IL-9 in patients with SLE and RA compared with controls and the association of IL-9 levels with clinical and laboratory parameters. IL-9 levels were assessed in 117 SLE patients, 67 RA patients, and 24 healthy controls by ELISA. Clinical and laboratory parameters were recorded. The IL-9 serum levels were significantly higher in RA patients (4,77 ± 3,618 pg/mL) and in SLE patients (12,26 ± 25,235 pg/mL) than in healthy individuals (1,22 ± 0,706 pg/mL)(p<0,001). In SLE patients, there were no statistically significant associations or correlations between the levels of IL-9 and SLEDAI or other clinical and laboratorial parameters, with the exception of disease time, which showed a statistically significant negative correlation with IL-9 levels(r=-0,1948; p=0,0378). In RA patients, no association or statistically significant correlation was observed with disease duration, DAS28, HAQ, rheumatoid factor positivity, or erosions on radiography. These data demonstrated increased serum levels of IL-9 in SLE and RA patients, but further studies are needed to clarify the precise role of this cytokine and its potential use as therapeutic target.

scholarly journals POS1250 VITAMIN D DEFICIENCY IS MAINLY ASSOCIATED WITH SEVERE LUNG INVOLVEMENT, LONGER DISEASE DURATION AND RISK OF DEATH IN ELDERLY COVID-19 PATIENTS

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 908.2-908
Author(s):  
A. Sulli ◽  
E. Gotelli ◽  
A. Casabella ◽  
M. Grosso ◽  
C. Schenone ◽  
...  
Keyword(s):  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Disease Duration ◽  
Serum Levels ◽  
Significant Negative Correlation ◽  
Pulmonary Involvement ◽  
Lung Involvement ◽  
Reactive Protein ◽  
Risk Of Death ◽  
Severe Lung

Background:Vitamin D regulates the innate and adaptive immune system responses and low vitamin D levels have been associated with the increased risk of respiratory tract infections (1). Vitamin D deficiency has been recently reported to interfere with the prognosis of COVID-19 (2,3).Objectives:The aim of this study was to correlate the 25OH-vitamin D serum levels with lung involvement and disease severity, in a cohort of elderly patients hospitalized for SARS-CoV-2 infection.Methods:Sixty-five COVID-19 patients (mean age 76±13 years) and sixty-five sex- and age-matched control subjects (CNT) were included in the study. Respiratory parameters (PaO2, SO2, PaCO2, PaO2/FiO2), clinical and laboratory parameters (including 25OH-vitamin D, D-dimer, C-reactive protein) and type of radiological pulmonary involvement were collected at hospital admission. Statistical analysis was performed by non-parametric tests.Results:Vitamin D sufficiency (>30 ng/ml), insufficiency (between 20 and 30 ng/ml), deficiency (between 10 and 20 ng/ml) and severe deficiency (<10 ng/ml) were observed respectively in 11, 11, 21 and 57 % of COVID-19 patients. Vitamin D serum levels were found significantly lower in COVID-19 patients than in CNT (median 8 vs 16 ng/ml, p=0.001). A statistically significant positive correlation was observed between vitamin D serum levels and SO2 (p=0.05), PaO2 (p=0.03), PaO2/FiO2 (p=0.02). A statistically significant negative correlation was found between vitamin D serum levels and severity of radiologic pulmonary involvement: vitamin D was significantly lower in COVID-19 patients with either diffuse/severe interstitial lung involvement (p=0.05) or multiple lung consolidations (p=0.0001) than in those with mild radiological lung involvement. Significantly lower vitamin D serum levels were found in COVID-19 patients who died during hospitalization, compared to those who survived (median 3 vs 8 ng/ml, p=0.05). Finally, a statistically significant negative correlation was found between vitamin D serum levels and D-dimer (p=0.04), C-reactive protein (p=0.04) and disease duration (p=0.05).Conclusion:This study confirms that severe vitamin D deficiency is associated with more severe lung involvement, longer disease duration and risk of death in elderly COVID-19 patients.References:[1]Cutolo M, et al. RMD Open. 2020; 6(3):e001454.[2]Bilezikian JP, et al. Eur J Endocrinol. 2020; 183(5):R133-R147.[3]Weir EK, et al. Clin Med (Lond). 2020; 20:e107-e108.Disclosure of Interests:None declared

scholarly journals IgE in the Pathogenesis of SLE: From Pathogenic Role to Therapeutic Target

Antibodies ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 69
Author(s):  
Yasmine Lamri ◽  
Nicolas Charles
Keyword(s):  
Lupus Erythematosus ◽  
Functional Outcomes ◽  
Allergic Diseases ◽  
Parasitic Infections ◽  
Pathogenic Role ◽  
Ige Antibodies ◽  
Therapeutic Modalities ◽  
Nuclear Antigens ◽  
Chronic Autoimmune Disease

Systemic lupus erythematosus (SLE) is a multifactorial chronic autoimmune disease, marked by the presence of autoantibodies to nuclear antigens belonging to different isotype classes. For several years, IgE antibodies have been incriminated in the development of allergic diseases and parasitic infections and different anti-IgE therapies have been developed to encounter the pathogenic role of IgE in these pathologies. Recently, multiple studies showed the presence of elevated total IgE levels and demonstrated a pathogenic role of autoreactive IgE in SLE. This review aims to summarize the findings incriminating IgE and autoreactive IgE in the pathophysiology of SLE, to describe their functional outcomes on their targeted cells as well as to discuss different IgE-related therapeutic modalities that emerged and that may be beneficial for SLE patient care.

scholarly journals Establishment of Monoclonal Anti-Retroviral gp70 Autoantibodies from MRL/lpr Lupus Mice and Induction of Glomerular gp70 Deposition and Pathology by Transfer into Non-Autoimmune Mice

2000 ◽  
Vol 74 (9) ◽  
pp. 4116-4126 ◽  
Author(s):  
Nobutada Tabata ◽  
Masaaki Miyazawa ◽  
Ryuichi Fujisawa ◽  
Yumiko A. Takei ◽  
Hiroyuki Abe ◽  
...  
Keyword(s):  
New Zealand ◽  
Immune Complexes ◽  
Severe Combined Immunodeficiency ◽  
Serum Levels ◽  
Gene Products ◽  
Linkage Studies ◽  
Pathogenic Role ◽  
Antinuclear Autoantibodies ◽  
Glomerular Lesions

ABSTRACT Several strains of mice, including MRL/MpJ mice homozygous for the Fas mutant lpr gene (MRL/lpr mice), F1 hybrids of New Zealand Black and New Zealand White mice, and BXSB/MpJ mice carrying a Y-linked autoimmune acceleration gene, spontaneously develop immune complex-mediated glomerulonephritis. The involvement of the envelope glycoprotein gp70 of an endogenous xenotropic virus in the formation of circulating immune complexes and their deposition in the glomerular lesions have been demonstrated, as has the pathogenicity of various antinuclear, antiphospholipid, and rheumatoid factor autoantibodies. In recent genetic linkage studies as well as in a study of cytokine-induced protection against nephritis development, the strongest association of serum levels of gp70–anti-gp70 immune complexes, rather than the levels of antinuclear autoantibodies, with the development and severity of glomerulonephritis has been demonstrated, suggesting a major pathogenic role of anti-gp70 autoantibodies in the lupus-prone mice. However, the pathogenicity of anti-gp70 autoantibodies has not yet been directly tested. To examine if anti-gp70 autoantibodies induce glomerular pathology, we established from unmanipulated MRL/lpr mice hybridoma clones that secrete monoclonal antibodies reactive with endogenous xenotropic viralenv gene products. Upon transplantation, a high proportion of these anti-gp70 antibody-producing hybridoma clones induced in syngeneic non-autoimmune and severe combined immunodeficiency mice proliferative or wire loop-like glomerular lesions. Furthermore, deposition of gp70 in glomeruli and pathological changes were observed after intravenous injection of representative clones of purified anti-gp70 immunoglobulin G, demonstrating pathogenicity of at least some anti-gp70 autoantibodies.

Is there any correlation between high sensitive CRP and disease activity in systemic lupus erythematosus?

Lupus ◽  
2011 ◽  
Vol 20 (14) ◽  
pp. 1494-1500 ◽  
Author(s):  
Z Rezaieyazdi ◽  
M Sahebari ◽  
MR Hatef ◽  
B Abbasi ◽  
H Rafatpanah ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Disease Activity ◽  
Lupus Erythematosus ◽  
Activity Index ◽  
Serum Levels ◽  
Enzyme Linked Immunosorbent Assay ◽  
Healthy Controls ◽  
Systemic Lupus ◽  
Hs Crp

The role of C-reactive protein (CRP) in systemic lupus erythematosus (SLE) as an inflammatory marker is still controversial. Recently, more sensitive methods, such as high sensitive CRP (hs-CRP) have been used to detect micro-inflammation. The role of hs-CRP in lupus flare has not been documented well. We conducted this study to examine the correlation between hs-CRP serum concentrations and disease activity in lupus. Ninety-two SLE patients and 49 healthy controls contributed to our study. Most confounding factors influencing the hs-CRP values were excluded. Disease activity was estimated using the SLE Disease Activity Index (SLEDAI-2K). hs-CRP values were determined using an enzyme-linked immunosorbent assay (ELISA) kit. Serum values of hs-CRP were significantly higher ( p < 0.001, z = 3.29) in patients compared with healthy controls. The cutoff point for hs-CRP between patients and controls was 0.93 mg/L (Youden’s Index = 0.39). There was no correlation between hs-CRP serum levels and disease activity. Furthermore, hs-CRP values did not correlate with any of the laboratory parameters, except for C3 ( p = 0.003, rs = −0.2) and C4 ( p = 0.02, rs = −0.1). Although hs-CRP serum levels were significantly higher in lupus patients compared with healthy controls, it seems that this marker is not a good indicator for disease activity.

scholarly journals Association of HMGB1, S100A12 and IL-17A Expression with IVIG-Resistant Kawasaki Disease and Treatment Options

2020 ◽  
Author(s):  
Deying Liu ◽  
Pan Liu ◽  
Fan Liu ◽  
Wei Yin ◽  
Yan Ding
Keyword(s):  
Kawasaki Disease ◽  
Coronary Arteries ◽  
Adjunctive Therapy ◽  
Clinical Symptoms ◽  
Treatment Options ◽  
Poor Response ◽  
Serum Levels ◽  
Laboratory Parameters ◽  
Molecular Pattern

Abstract Background: Kawasaki disease (KD) is a medium vessel vasculitis of unknown aetiology that predominantly affecting coronary arteries. The damage-associated molecular pattern molecules (DAMPs) such as HMGB1, S100A12 and IL-17A have been reported to predict poor response to IVIG. Here, we explored the the role of HMGB1, S100A12 and IL-17A in the detection of intravenous immunoglobulin (IVIG)-resistant in KD patients, and to investigate the value of different adjunctive therapy.Method: 126 KD patients and as well as age- and sex-matched 16 febrile control subjects were enrolled in our study. The fresh peripheral blood were collected from KD patients and febrile controls, analyzed the demographic or clinical data and various laboratory parameters. We also measured changes in serum levels of IL-17A and mRNA expression levels of HMGB1 and S100A12 were tested in IVIG-resistant KD patients. Further we explored the association between coronary arteries lesions and different treatment options about IVIG retreatment, methylprednisolone and infliximab for IVIG-resistant KD patients. Result: Regarding laboratory parameters, KD individuals were found to have lower levels of lymphocyte(L)%, prealbumin, CD4+, CD8+ and higher levels of WBC, neutrophil (N)%, CRP, ESR, NT-proBNP, ALT, CD4+/CD8+ (P<0.05 or P<0.01). For KD group, the 53 IVIG-resistant patients had significantly higher levels of S100A12, HMGB1, serum IL-17A, N%, CRP, NT-proBNP, TBIL, ALT, AST and lower levels of L%, PLT (P<0.05 or P<0.01) in comparison to the IVIG-responsive patients. For patients with IVIG-resistant, IVIG retreatment, methylprednisolone or infliximab were used. Methylprednisolone showed better in improving clinical symptoms and CRP than the IVIG retreatment and infliximab (P> 0.05).Conclusion: IVIG-resistant was associated with overreaction of inflammation.The levels of HMGB1,S100A12 and IL-17A suggested to be reliable predictors for IVIG-resistant in KD. In addition, the adjunctive therapy of methylprednisolone and infliximab showed more effective in relieving clinical symptoms than IVIG retreatment.

scholarly journals Interleukin (IL)-1 family cytokine in primary immune thrombocytopenia: a comparison with systemic lupus erythematosus-associated thrombocytopenia

2020 ◽  
Author(s):  
Yanxia Zhan ◽  
Boting Wu ◽  
Chanjuan liu ◽  
Luya Cheng ◽  
Lili Ji ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Platelet Count ◽  
Lupus Erythematosus ◽  
Immune Thrombocytopenia ◽  
Serum Levels ◽  
Healthy Controls ◽  
Systemic Lupus ◽  
Primary Immune Thrombocytopenia ◽  
Polymerase Chain

Abstract Background : Primary immune thrombocytopenia (ITP) is an autoimmune-mediated disorder characterized by decreased platelet count. Systemic lupus erythematosus (SLE) is also an autoimmune disease which thrombocytopenia is a common hematologic manifestation. Interleukin (IL)-1 family cytokines are major proinflammatory and immunoregulatory mediators. This study aimed to investigate the role of IL-1 cytokines in patients with ITP and SLE and the potential pathophysiologic mechanism to differentiate SLE-associated thrombocytopenia (SLE-TP) from ITP. Methods : Multiplex cytokine assay and real-time polymerase chain reaction (RT-PCR) were used to measure the IL-1 cytokines in 17 newly diagnosed ITP patients, 17 SLE-TP patients, 19 SLE patients without thrombocytopenia (SLE-NTP) and 10 healthy controls. Results : The serum levels of IL-1β, IL-18, IL-36α, IL-36β, IL-36γ and IL-33 were decreased significantly in ITP patients as compared with SLE-TP, SLE-NTP patients and healthy controls ( p <0.05). There was no significantly difference in the serum level of IL-37 between ITP and SLE-TP patients, however, there is a positive correlation between platelet count with IL-37 level in ITP patients. Our data suggested that serum IL-1β, IL-18, IL-36α, IL-36β, IL-36γ, IL-33 and IL-37 were involved in the pathogenesis of ITP. Conclusions : Serum IL-1β, IL-18, IL-36α, IL-36β, IL-36γ and IL-33 could be considered biomarkers to differentiate SLE-TP from ITP patients.

scholarly journals Association of HMGB1, S100A12 and IL-17A Expression with Immunoglobulin-Resistant in Kawasaki Disease and the Comparisons Between Different Adjunctive Therapeutic Approaches

2022 ◽  
Author(s):  
Yang Zhou ◽  
Liu Pan ◽  
You-jun Yang ◽  
Shi-yu Li ◽  
Wei Yin ◽  
...  
Keyword(s):  
Adjunctive Therapy ◽  
Clinical Symptoms ◽  
Poor Response ◽  
Serum Levels ◽  
Ivig Treatment ◽  
Control Group ◽  
Laboratory Parameters ◽  
Methyl Prednisolone ◽  
Laboratory Variables

Abstract Objective: The DAMPs such as HMGB1, S100A12 and IL-17A have been reported to predict poor response to IVIG. The aim of this study was to analyze the role of HMGB1,S100A12 and IL-17A in the detection of inflammation in KD patients with IVIG-resistant, and to investigate the value of different adjunctive therapy.Method: This study enrolled 126 patients diagnosed with KD, as well as age-matched 16 febrile control subjects. The demographic or clinical data, laboratory parameter and blood sample were collected. Various laboratory parameters as predictive factors for IVIG-resistant were calculated. And the serum levels of IL-17A and mRNA expression levels of HMGB1 and S100A12 were tested in all patients. For patients with acute KD in IVIG-resistant, we studied the levels of laboratory variables when using of IVIG retreatment, methylprednisolone, infliximab for children patients. Result: The variance of laboratory parameters between the febrile control group and KD group were analyzed. Regarding laboratory parameters, KD individuals were found to have lower levels of L%, PA, CD4+, CD8+ and higher levels of WBC, N%, CRP, ESR, NT-proBNP, ALT, CD4+/CD8+ (P<0.05 or P<0.01). For KD group, the 53 IVIG-resistant patients had significantly higher levels of blood S100A12, HMGB1, serum IL-17A levels And N%, CRP, NT-pro BNP, TBIL, ALT, AST and lower levels of L%, PLT (P<0.05 or P<0.01) in comparison to the IVIG-responsive patients. For patients with acute KD in IVIG-resistant, after initial IVIG-treatment, the adjunctive therapy of IVIG, methyl prednisolone or infliximab were used, the inflammatory symptoms and laboratory inflammatory markers were improved when treated with those drugs. Conclusion: IVIG-resistant was associated with higher levels of HMGB1, S100A12, IL-17A, CRP, NT-pro BNP, TBIL, ALT, AST and lower levels of L%, PLT before IVIG, especially when combined, were useful predictors for IVIG-resistant in KD. In addition, the adjunctive therapy of methylprednisolone and infliximab showed more effective in relief clinical symptoms than IVIG retreatment.

scholarly journals High levels of gut-homing immunoglobulin A–positive+B lymphocytes support the pathogenic role of intestinal mucosal hyperresponsiveness in immunoglobulin A nephropathy patients

2020 ◽  
Author(s):  
Fabio Sallustio ◽  
Claudia Curci ◽  
Nada Chaoul ◽  
Giulia Fontò ◽  
Gabriella Lauriero ◽  
...  
Keyword(s):  
B Cells ◽  
B Lymphocytes ◽  
Immunoglobulin A ◽  
Serum Levels ◽  
Memory B Cells ◽  
Immunoglobulin A Nephropathy ◽  
Pathogenic Role ◽  
Significant Difference ◽  
Activated B Cells

Abstract Background Immunoglobulin A nephropathy (IgAN) is the most frequent primary glomerulonephritis. The role of the microbiota and mucosal immunity in the pathogenesis of IgAN remains a key element. To date, the hypothetical relationship between commensal bacteria, elevated tumour necrosis factor (TNF) superfamily member 13 [also known as B-cell activating factor (BAFF)] levels, perturbed homoeostasis of intestinal-activated B cells and intestinal IgA class switch has not been clearly shown in IgAN patients. Methods We studied the intestinal–renal axis connections, analysing levels of BAFF, TNF ligand superfamily member 13 (APRIL) and intestinal-activated B cells in IgAN patients, healthy subjects (HSs) and patients with non-IgA glomerulonephritides. Results IgAN patients had increased serum levels of BAFF cytokine, correlating with higher amounts of five specific microbiota metabolites, and high APRIL cytokine serum levels. We also found that subjects with IgAN have a higher level of circulating gut-homing (CCR9+ β7 integrin+) regultory B cells, memory B cells and IgA+ memory B cells compared with HSs. Finally, we found that IgAN patients had high levels of both total plasmablasts (PBs) and intestinal-homing PBs. Interestingly, PBs significantly increased in IgAN but not in patients with other glomerulonephritides. Conclusions Our results demonstrate a significant difference in the amount of intestinal-activated B lymphocytes between IgAN patients and HSs, confirming the hypothesis of the pathogenic role of intestinal mucosal hyperresponsiveness in IgAN. The intestinal–renal axis plays a crucial role in IgAN and several factors may contribute to its complex pathogenesis and provide an important area of research for novel targeted therapies to modulate progression of the disease.

scholarly journals Blocking IL-17: A Promising Strategy in the Treatment of Systemic Rheumatic Diseases

2020 ◽  
Vol 21 (19) ◽  
pp. 7100
Author(s):  
Carlos Rafael-Vidal ◽  
Nair Pérez ◽  
Irene Altabás ◽  
Samuel Garcia ◽  
Jose M. Pego-Reigosa
Keyword(s):  
Rheumatic Diseases ◽  
Lupus Erythematosus ◽  
Therapeutic Option ◽  
Premature Mortality ◽  
Interleukin 17 ◽  
Multiple Organs ◽  
Systemic Rheumatic Diseases ◽  
Bacteria And Fungi ◽  
Potential Use

Systemic rheumatic diseases are a heterogeneous group of autoimmune disorders that affect the connective tissue, characterized by the involvement of multiple organs, leading to disability, organ failure and premature mortality. Despite the advances in recent years, the therapeutic options for these diseases are still limited and some patients do not respond to the current treatments. Interleukin-17 (IL-17) is a cytokine essential in the defense against extracellular bacteria and fungi. Disruption of IL-17 homeostasis has been associated with the development and progression of rheumatic diseases, and the approval of different biological therapies targeting IL-17 for the treatment of psoriatic arthritis (PsA) and ankylosing spondylitis (AS) has highlighted the key role of this cytokine. IL-17 has been also implicated in the pathogenesis of systemic rheumatic diseases, including systemic lupus erythematosus (SLE), Sjögren’s syndrome (SS) and systemic sclerosis (SSc). The aim of this review is to summarize and discuss the most recent findings about the pathogenic role of IL-17 in systemic rheumatic and its potential use as a therapeutic option.

Role of MMP-2 and its inhibitor TIMP-2 as biomarkers for susceptibility to systemic lupus erythematosus

2020 ◽  
Vol 14 (12) ◽  
pp. 1109-1119
Author(s):  
Hemant J Vira ◽  
Vandana D Pradhan ◽  
Vinod D Umare ◽  
Ajay K Chaudhary ◽  
Anjali G Rajadhyksha ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Serum Level ◽  
Mrna Expression ◽  
Lupus Erythematosus ◽  
Serum Levels ◽  
Healthy Controls ◽  
Systemic Lupus ◽  
Functional Polymorphisms ◽  
Pcr Rflp

Aim: To investigate the possible association between MMP-2 (−1575 G/A, −1306 C/T) and its inhibitor TIMP-2 (−418 G/C) functional polymorphisms with development of severity in systemic lupus erythematosus (SLE) patients. Materials & methods: 150 SLE patients and matched healthy controls were recruited. Polymorphisms were detected by PCR-RFLP and serum levels by ELISA. Results: Mean MMP-2 and TIMP-2 serum level and mRNA expression were significantly increased in SLE cases as compared with controls (p < 0.0001). The concomitant presence of both MMP-2 1575A and its inhibitor TIMP-2 418C alleles synergistically increased the risk of SLE by 3.25-fold (CI: 1.44–7.34, p = 0.003). Conclusion: MMP-2, TIMP-2 and MMP-2/TIMP-2 ratios may act as biomarkers for susceptibility to SLE.

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