Retraction Note: Arthritis Res Ther 13, R130 (2011)
https://doi.org/10.1186/ar3441
The Editors-in-Chief have retracted this article because an investigation jointly conducted by Rush University and the Jesse Brown Veterans Affairs Medical Center (JBVAMC) has determined that Fig. 5B contains fabricated and/or falsified data. Gillian Murphy agrees with this retraction. Simon M. Cool, Andre J. van Wijnen, Katalin Mikecz and Hee-Jeong Im have not responded to correspondence from the Publisher about this retraction. The Publisher has not been able to find current email addresees for Dongyao Yan and Di Chen.
Department of Biochemistry, Rush University Medical Center, 1735 W Harrison Street, Chicago, IL, 60612, USA
Dongyao Yan, Di Chen & Hee-Jeong Im
Department of Internal Medicine, Section of Rheumatology, Rush University Medical Center, 1735 W Harrison Street, Chicago, IL, 60612, USA
Hee-Jeong Im
Orthopedic Surgery, Rush University Medical Center, 1735 W Harrison Street, Chicago, IL, 60612, USA
Katalin Mikecz & Hee-Jeong Im
Department of Bioengineering, University of Illinois, 1304 West Springfield Avenue, Chicago, IL, 60612, USA
Hee-Jeong Im
Department of Stem Cells and Tissue Repair, Institute of Medical Biology, A*STAR, 8A Biomedical Grove, #06-06, Immunos, Singapore, 138648, Singapore
Simon M Cool
Division of Musculoskeletal Oncology, Department of Orthopaedic Surgery, Yong Loo Lin School of Medicine, National University of Singapore, 5 Lower Kent Ridge Road, Singapore, 119074, Singapore
Simon M Cool & Andre J van Wijnen
Department of Cell Biology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA, 01655, USA
Andre J van Wijnen
Department of Oncology, Cambridge University, Cancer Research Institute, Li Ka Shing Center, Robinson Way, CB2 ORE, Cambridge, 60612, UK
Gillian Murphy
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Introduction: IL-40 is a novel cytokine associated with autoimmune connective tissue disorders such as rheumatoid arthritis (RA) or Sjögren syndrome. We have previously shown an accumulation of IL-40 in the RA joint and its expression by immune cells and fibroblasts. Therefore, we aimed to assess the role of IL-40 in association with hyaline cartilage and chondrocyte activity.
Methods: Immunohistochemistry was employed to detect IL-40 in paired samples of loaded and unloaded regions of osteoarthritis (OA) cartilage (n=5). Synovial fluid IL-40 was analysed by ELISA in OA (n=31) and control individuals after knee injury (n=34). The impact of IL-40 on chondrocytes was tested in vitro.
Results: IL-40 was found in chondrocytes of the superficial zone of the OA cartilage, both in loaded and unloaded explants. Additionally, only biopsies from loaded explants showed significant IL-40 positivity in transitional zone chondrocytes. Levels of IL-40 were significantly elevated in the synovial fluid from OA patients compared to controls (p<0.0009) and correlated with synovial fluid leukocyte counts in OA (r=0.444, p=0.014). Chondrocytes exposed to IL-40 dose dependently increased in the secretion of pro-inflammatory cytokines IL-6 (p<0.0001) and IL-8 (p=0.004). Moreover, a dose dependent up-regulation of matrix degrading metalloproteinases MMP-1 (p=0.004), MMP-3 (p=0.031) and MMP-13 (p=0.0002) upon IL-40 treatment was observed in contrast to untreated chondrocytes.
Conclusion: This study is the first to demonstrate the accumulation of IL-40 in OA cartilage and its up-regulation in the synovial fluid of OA patients compared to controls. In addition, extracellular IL-40 appears to play a role in promoting inflammation and cartilage destruction by driving chondrocyte behaviour towards a more aggressive phenotype.
Background: Rheumatoid arthritis (RA) patients sometimes exhibit different levels of improvement in health assessment questionnaire-disability index (HAQ-DI) and subjective pain visual analogue score (VAS) even after achieving low disease activities (LDA). This study aimed to identify factors associated with improvement in HAQ-DI and pain VAS among those who achieved LDA.
Methods: Data of the FIRST registry, a multi-institutional cohort of RA patients treated with biological and targeted-synthetic DMARDs (b/tsDMARDs) were analyzed. Patients who were enrolled from August 2013 to February 2023 and who achieved clinical LDA [clinical disease activity index (CDAI) ≤ 10.0] at 6 months after starting treatment were included. Multiple logistic regression analyses were conducted to identify the factors that associated with achieving HAQ-DI normalization (< 0.5), HAQ-DI improvement (by > 0.22), or pain VAS reduction (≤ 40 mm).
Results: Among 1424 patients who achieved LDA at 6 months, 732 patients achieved HAQ-DI normalization and 454 achieved pain VAS reduction. The seropositivity and the use of JAK inhibitor compared with TNF inhibitor were associated with both HAQ-DI < 0.5 and pain VAS reduction at 6 months. On the other hand, older age, past failure in ≥ 2 classes of b/tsDMARDs, higher HAQ-DI at baseline, and use of glucocorticoid were associated with the lower likelihood of HAQ-DI normalization and pain VAS reduction. Longer disease duration, being female, and higher disease activity at baseline was negatively associated HAQ-DI normalization alone. Comorbidities were not associated with the outcomes.
Conclusions: These results suggest some preferable treatment may exist for improvement of HAQ-DI and pain VAS reduction in the early stage of the treatment, which is a clue to prevention of a criteria of difficult-to-treat RA.
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