Pitfalls for detecting interleukin-33 by ELISA in the serum of patients with primary Sjögren syndrome: comparison of different kits

Rivière, Élodie; Ly, Bineta; Boudaoud, Saida; Chavez, Houria; Nocturne, Gaëtane; Chanson, Philippe; Richard, Corinne Miceli; Mariette, Xavier

doi:10.1136/annrheumdis-2015-208557

Cited by 21 publications

(16 citation statements)

References 3 publications

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“…Since the IL-33 protein may be easily quantified in the serum, we first assessed serum IL-33 levels in the same population using the DuoSet ELISA IL-33 kit (R&D System) and preliminary reported in an abstract that the serum IL-33 level was associated with the RTX response [23]. However, additional experiments in patients with Sjögren’s syndrome or RA have raised caution about the accuracy of this kit for sera measurements [24]. Consequently, we discarded these preliminary results and examined serum IL-33 again with an accurate ELISA kit (Quantikine) validated for sera, in two separate and then merged populations.…”

Section: Discussionmentioning

confidence: 99%

“…However, this kit was not validated for human sera and additional experiments have confirmed the need for caution about the accuracy of this kit for sera measurements [24]. Recommendations from the manufacturer advise us to use another assay for human sera, named Quantikine and also provided by R&D Systems.…”

Section: Methodsmentioning

confidence: 99%

“…Using a sample obtained prior to the initiation of RTX in the two cohorts, we measured the serum IL-33 level using the Quantikine kit, which is a solid-phase ELISA with a 6.25 pg/mL lower limit threshold according to the manufacturer’s instruction [24]. The assessment of rheumatoid factor (RF), anti-cyclic citrullinated peptide (anti-CCP) antibodies, and serum IgG level were also performed.…”

Section: Methodsmentioning

confidence: 99%

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Serum IL-33, a new marker predicting response to rituximab in rheumatoid arthritis

et al. 2016

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BackgroundRecent works have suggested a possible link between interleukin (IL)-33 and B-cell biology. We aimed to study the possible association between serum IL-33 detection and response to rituximab (RTX) in rheumatoid arthritis (RA) patients in different cohorts with an accurate enzyme-linked immunosorbent assay (ELISA).MethodsSerum IL-33, rheumatoid factor (RF), anti-cyclic citrullinated peptide (anti-CCP), and high serum immunoglobulin (Ig)G levels were assessed in 111 RA patients receiving a first course of 2 g RTX (cohort 1) in an observational study and in 74 RA patients treated with the same schedule in routine care (cohort 2). Univariate and multivariate analyses identified factors associated with a European League Against Rheumatism (EULAR) response at 24 weeks.ResultsAt week 24, 84/111 (76%) and 54/74 (73%) patients reached EULAR response in cohorts 1 and 2, respectively. Serum IL-33 was detectable in only 33.5% of the patients. In the combined cohorts, the presence of RF or anti-CCP (odds ratio (OR) 3.27, 95% confidence interval (CI) 1.13–9.46; p = 0.03), high serum IgG (OR 2.32, 95% CI 1.01–5.33; p = 0.048), and detectable serum IL-33 (OR 2.40, 95% CI 1.01–5.72; p = 0.047) were all associated with RTX response in multivariate analysis. The combination of these three factors increased the likelihood of response to RTX. When serum IL-33 detection was added to seropositivity and serum IgG level, 100% of the patients with the three risk factors (corresponding to 9% of the population) responded to RTX (OR versus patients with none of the three risk factors 29.61, 95% CI 1.30–674.79; p = 0.034).ConclusionDetectable serum IL-33 may predict clinical response to RTX independently of, and synergistically with, auto-antibodies and serum IgG level.Trial registration NCT01126541; 18 May 2010.Electronic supplementary materialThe online version of this article (doi:10.1186/s13075-016-1190-z) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Serum IL-33, a new marker predicting response to rituximab in rheumatoid arthritis

et al. 2016

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“…To rule out the possibility that cleaved forms of IL-33 were undetected in our assays and improve the recently proposed reliability issue of human IL-33 ELISA kit 41 , we used a complementary ELISA kit that analysed the presence of the C-terminal epitope of IL-33, in addition to an ELISA kit used in a previous study 2, 4 . Both kits showed the same results, i.e.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-33 regulates intestinal inflammation by modulating macrophages in inflammatory bowel disease

Seo

Che

Kwak

et al. 2017

Sci Rep

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Interleukin 33 (IL-33) that signals through the ST2 receptor has emerged as a critical modulator in several inflammatory disorders, including inflammatory bowel disease (IBD). However, the precise mechanisms by which IL-33 modulates IBD are controversial. The aim of this study was thus to clarify the role of IL-33 in IBD. The plasma levels of IL-33 were significantly decreased, but soluble ST2 levels were increased in patients with IBD compared to healthy individuals. Moreover, IL-33 restored goblet cell numbers and induced macrophage switching from the M1 to the M2 phenotype. These effects were sufficient to ameliorate colitis in dextran sodium sulfate, trinitrobenzene sulfonic acid, and peritoneal cavity cell transfer models. IL-33 facilitated goblet cell restoration via modulating macrophages toward the M2 phenotype. In addition, wound healing was significantly faster in IL-33-treated human monocyte-derived macrophages than in control cells, which could be attributed to increased polarisation into M2 macrophages. We found that patients with IBD show decreased serum levels of IL-33 compared with healthy individuals and that IL-33 can attenuate colitis and aid tissue repair in mice. The mechanism by which IL-33 exerts these effects appears to involve the stimulation of differentiation of goblet cells and M2 macrophages.

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“…Detection of IL-33 levels in a human fluid specimen largely relies on commercially available ELISA kits. Several studies, however, have demonstrated that the measurement of serum concentrations of IL-33 is challenging and may produce false positive results, which is a caveat for further investigations with serum samples [102,103,104]. The correlation between serum IL-33 levels and impaired renal function remains controversial; nevertheless, upregulation of tissue IL-33 levels is generally consistent in different renal injury models (Table 1).…”

Section: Discussionmentioning

confidence: 99%

Emerging Roles of IL-33/ST2 Axis in Renal Diseases

Chen

Yang

2017

IJMS

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Renal diseases, including acute kidney injury (AKI) and chronic kidney disease (CKD), have a great impact on health care systems worldwide. Similar to cardiovascular diseases, renal diseases are inflammatory diseases involving a variety of cytokines. Primary causes of renal injury include ischemia, uremic toxins, bacteremia, or nephrotoxicity. Inflammation represents an important component following kidney injury. Interleukin (IL)-33 is a member of the IL-1 cytokine family, which is widely expressed in epithelial barrier tissues and endothelial cells, and mediates both tissue inflammation and repair responses. IL-33 is released as a nuclear alarmin in response to tissue damage and triggers innate and adaptive immune responses by binding to its receptor, suppression of tumorigenicity 2 (ST2). Recent evidence from clinical and experimental animal studies indicates that the IL-33/ST2 axis is involved in the pathogenesis of CKD, renal graft injury, systemic lupus nephritis, and AKI. In this review, we discuss the pathological and tissue reparative roles of the IL-33/ST2 pathway in different types of renal diseases.

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Pitfalls for detecting interleukin-33 by ELISA in the serum of patients with primary Sjögren syndrome: comparison of different kits

Cited by 21 publications

References 3 publications

Serum IL-33, a new marker predicting response to rituximab in rheumatoid arthritis

Serum IL-33, a new marker predicting response to rituximab in rheumatoid arthritis

Interleukin-33 regulates intestinal inflammation by modulating macrophages in inflammatory bowel disease

Emerging Roles of IL-33/ST2 Axis in Renal Diseases

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