| Peer-Reviewed

Elevated Level of Interleukin-29: A Proinflammatory Role in Synovial Inflammation of Rheumatoid Arthritis

Received: 13 March 2014    Accepted: 9 April 2014    Published: 20 April 2014
Views:       Downloads:
Abstract

Background: The multiple pro-inflammatory cascades described in RA lead to persistent synovitis, resulting in articular cartilage and bone damages. The up-regulation of interferon-inducible genes has been found in the synovial lining regions and may play an important role in the pathogenesis of RA. Objective: The aim of the current study is to examine the expression of IL-29 and its receptors IL-28Rα in blood and synovial fluid (SF) in RA patients and investigate the correlation of IL-29 with disease activity and other laboratory characters of RA. Methods: The study was carried out on 108 RA patients, 70 OA patients and 80 healthy control subjects. Clinical assessment of disease activity in RA patients and disease activity score with DAS28 had been done. IL29 was detected in the serum and synovial fluid of all samples by ELISA. Real time PCR was used for human IL-29 and IL-28Rα expression from PBMC. Results: expression of IL-29 mRNA was significantly higher in RA PBMCs when compared to OA and HC (132±13.8, 49± 11.2, 33.3± 10.5; respectively P <0.05). Similarly, IL-28Rα mRNA expression was significantly higher in RA PBMCs when compared to OA and HC (30.5±9.7, 13.3±4.5, 8.5± 3.3; respectively P <0.05). The mean level of IL-29 in SF was increased in RA and found also much higher in RA (17.29 ± 10.19pg/ml) than OA (8.33 ±3.89 pg/ml) (P = 0.01). There is a significant correlation between serum levels of circulating IL- 29 and DAS28, CRP, ESR, RF, and anti-CCP. Conclusion: our data have presented new evidence that IL-29 may contribute to RA pathogenesis

Published in Advances in Biochemistry (Volume 2, Issue 2)
DOI 10.11648/j.ab.20140202.11
Page(s) 29-33
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

IL29, Rheumatoid Arthritis, Synovial Inflammation

References
[1] Scott DL, Wolfe F, Huizinga TW. Rheumatoid arthritis. Lancet 2010, 376: 1094–1108.
[2] Brennan FM, McInnes IB. Evidence that cytokines play a role in rheumatoid arthritis. J Clin Invest 2008, 118: 3537–3545.
[3] Yoshida S, Arakawa F, Higuchi F, Ishibashi Y, Goto M, et al. Gene expression analysis of rheumatoid arthritis synovial lining regions by cDNA microarray combined with laser microdissection: up-regulation of inflammation-associated STAT1, IRF1, CXCL9, CXCL10, and CCL5. Scand J Rheumatol 2012, 41:170-179.
[4] Higgs BW, Zhu W, Richman L, Fiorentino DF, Greenberg SA et al. Identification of activated cytokine pathways in the blood of systemic lupus erythematosus, myositis, rheumatoid arthritis, and scleroderma patients. Int J Rheum Dis 2012, 15:25-35.
[5] Witte K, Witte E, Sabat R, Wolk K: IL-28A, IL-28B, and IL-29: promising cytokines with type I interferon-like properties. Cytokine Growth Factor Rev 2010, 21:237–251.
[6] Kotenko SV: IFN-λs. Curr Opin Immunol 2011, 23:583–590.
[7] Diegelmann J, Beigel F, Zitzmann K, Kaul A, G?ke B,et al. Comparative analysis of the lambda-interferons IL-28A and IL-29 regarding their transcriptome and their antiviral properties against hepatitis C virus. PLoS One. 2010, Volume 5 | Issue 12 | e15200
[8] Honda K, Takaoka A, Taniguchi T. Type I interferon (corrected) gene induction by the interferon regulatory factor family of transcription factors. Immunity. 2006;25:349–360
[9] Donnelly RP, Kotenko SV: Interferon-λ: a new addition to an old family. J Interferon Cytokine Res 2010, 30:555–564.
[10] Zhang L, Jilg N, Shao RX, Lin W, Fusco DN, et al: IL28B inhibits hepatitis C virus replication through the JAK-STAT pathway. J Hepatol 2011, 55:289–298.
[11] Liu MQ, Zhou DJ, Wang X, Zhou W, Ye L, et al: IFN-λ3 inhibits HIV infection of macrophages through the JAK-STAT pathway. PLoS One 2012, 7:e35902.
[12] van Tuyl LH, Vlad SC, Felson DT, Wells G, Boers M: Defining remission in rheumatoid arthritis: results of an initial American College of Rheumatology/European League Against Rheumatism consensus conference. Arthritis Rheum 2009, 61:704-710.
[13] Witte K, Witte E, Sabat R, Wolk K. IL-28A, IL-28B, and IL-29: promising cytokines with type I interferon-like properties. Cytokine Growth Factor Rev. 2010 Aug;21(4):237-51. doi: 10.1016/j.cytogfr.2010.04.002. Epub 2010 Jul 23.
[14] Wang F, Xu L, Feng X, Guo D, Tan W, et al. Interleukin-29 modulates proinflammatory cytokine production in synovial inflammation of rheumatoid arthritis. Arthritis Res Ther. 2012 Oct 19; 14(5):R228.
[15] McInnes IB, Schett G. Cytokines in the pathogenesis of rheumatoid arthritis. Nat Rev Immunol 2007; 7:429- 42.
[16] Firestein GS. Evolving concepts of rheumatoid arthritis. Nature 2003; 423:356- 61.
[17] Choy E. Understanding the dynamics: pathways involved in the pathogenesis of rheumatoid arthritis. Rheumatology 2012;51:v3- v11 doi:10.1093/rheumatology/kes113
[18] Smolen JS, Steiner G. Therapeutic strategies for rheumatoid arthritis. Nat Rev Drug Discov 2003;2:473- 88.
[19] Xu L, Feng X, Tan W, Gu W, Guo D, et al. IL-29 enhances Toll-like receptor-mediated IL-6 and IL-8 production by the synovial fibroblasts from rheumatoid arthritis patients. Arthritis Res Ther. 2013 Oct 29; 15(5):R170. doi: 10.1186/ar4357.
[20] Jordan WJ, Eskdale J, Boniotto M, Rodia M, Kellner D, et al: Modulation of the human cytokine response by interferon λ-1 (IFN-λ1/IL-29). Genes Immun 2007, 8:13–20.
[21] Hashizume.M and Mihara.M: The Roles of Interleukin-6 in the Pathogenesis of Rheumatoid Arthritis. Arthritis. 2011; 2011:765624. doi: 10.1155/2011/765624. Epub 2011 May 26.
[22] Dayer JM, Choy E. Therapeutic targets in rheumatoid arthritis: the interleukin-6 receptor. Rheumatology 2010; 49:15- 24.
[23] Smolen JS, Aletaha D, Koeller M, Weisman MH, Emery P. New therapies for treatment of rheumatoid arthritis. Lancet 2007; 370:1861- 74.
Cite This Article
  • APA Style

    Dalia A. Shaheen, Hisham M. Habib. (2014). Elevated Level of Interleukin-29: A Proinflammatory Role in Synovial Inflammation of Rheumatoid Arthritis. Advances in Biochemistry, 2(2), 29-33. https://doi.org/10.11648/j.ab.20140202.11

    Copy | Download

    ACS Style

    Dalia A. Shaheen; Hisham M. Habib. Elevated Level of Interleukin-29: A Proinflammatory Role in Synovial Inflammation of Rheumatoid Arthritis. Adv. Biochem. 2014, 2(2), 29-33. doi: 10.11648/j.ab.20140202.11

    Copy | Download

    AMA Style

    Dalia A. Shaheen, Hisham M. Habib. Elevated Level of Interleukin-29: A Proinflammatory Role in Synovial Inflammation of Rheumatoid Arthritis. Adv Biochem. 2014;2(2):29-33. doi: 10.11648/j.ab.20140202.11

    Copy | Download

  • @article{10.11648/j.ab.20140202.11,
      author = {Dalia A. Shaheen and Hisham M. Habib},
      title = {Elevated Level of Interleukin-29: A Proinflammatory Role in Synovial Inflammation of Rheumatoid Arthritis},
      journal = {Advances in Biochemistry},
      volume = {2},
      number = {2},
      pages = {29-33},
      doi = {10.11648/j.ab.20140202.11},
      url = {https://doi.org/10.11648/j.ab.20140202.11},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ab.20140202.11},
      abstract = {Background: The multiple pro-inflammatory cascades described in RA lead to persistent synovitis, resulting in articular cartilage and bone damages. The up-regulation of interferon-inducible genes has been found in the synovial lining regions and may play an important role in the pathogenesis of RA. Objective: The aim of the current study is to examine the expression of IL-29 and its receptors IL-28Rα in blood and synovial fluid (SF) in RA patients and investigate the correlation of IL-29 with disease activity and other laboratory characters of RA. Methods: The study was carried out on 108 RA patients, 70 OA patients and 80 healthy control subjects. Clinical assessment of disease activity in RA patients and disease activity score with DAS28 had been done. IL29 was detected in the serum and synovial fluid of all samples by ELISA. Real time PCR was used for human IL-29 and IL-28Rα expression from PBMC. Results: expression of IL-29 mRNA was significantly higher in RA PBMCs when compared to OA and HC (132±13.8, 49± 11.2, 33.3± 10.5; respectively P <0.05). Similarly, IL-28Rα mRNA expression was significantly higher in RA PBMCs when compared to OA and HC (30.5±9.7, 13.3±4.5, 8.5± 3.3; respectively P <0.05). The mean level of IL-29 in SF was increased in RA and found also much higher in RA (17.29 ± 10.19pg/ml) than OA (8.33 ±3.89 pg/ml) (P = 0.01). There is a significant correlation between serum levels of circulating IL- 29 and DAS28, CRP, ESR, RF, and anti-CCP. Conclusion: our data have presented new evidence that IL-29 may contribute to RA pathogenesis},
     year = {2014}
    }
    

    Copy | Download

  • TY  - JOUR
    T1  - Elevated Level of Interleukin-29: A Proinflammatory Role in Synovial Inflammation of Rheumatoid Arthritis
    AU  - Dalia A. Shaheen
    AU  - Hisham M. Habib
    Y1  - 2014/04/20
    PY  - 2014
    N1  - https://doi.org/10.11648/j.ab.20140202.11
    DO  - 10.11648/j.ab.20140202.11
    T2  - Advances in Biochemistry
    JF  - Advances in Biochemistry
    JO  - Advances in Biochemistry
    SP  - 29
    EP  - 33
    PB  - Science Publishing Group
    SN  - 2329-0862
    UR  - https://doi.org/10.11648/j.ab.20140202.11
    AB  - Background: The multiple pro-inflammatory cascades described in RA lead to persistent synovitis, resulting in articular cartilage and bone damages. The up-regulation of interferon-inducible genes has been found in the synovial lining regions and may play an important role in the pathogenesis of RA. Objective: The aim of the current study is to examine the expression of IL-29 and its receptors IL-28Rα in blood and synovial fluid (SF) in RA patients and investigate the correlation of IL-29 with disease activity and other laboratory characters of RA. Methods: The study was carried out on 108 RA patients, 70 OA patients and 80 healthy control subjects. Clinical assessment of disease activity in RA patients and disease activity score with DAS28 had been done. IL29 was detected in the serum and synovial fluid of all samples by ELISA. Real time PCR was used for human IL-29 and IL-28Rα expression from PBMC. Results: expression of IL-29 mRNA was significantly higher in RA PBMCs when compared to OA and HC (132±13.8, 49± 11.2, 33.3± 10.5; respectively P <0.05). Similarly, IL-28Rα mRNA expression was significantly higher in RA PBMCs when compared to OA and HC (30.5±9.7, 13.3±4.5, 8.5± 3.3; respectively P <0.05). The mean level of IL-29 in SF was increased in RA and found also much higher in RA (17.29 ± 10.19pg/ml) than OA (8.33 ±3.89 pg/ml) (P = 0.01). There is a significant correlation between serum levels of circulating IL- 29 and DAS28, CRP, ESR, RF, and anti-CCP. Conclusion: our data have presented new evidence that IL-29 may contribute to RA pathogenesis
    VL  - 2
    IS  - 2
    ER  - 

    Copy | Download

Author Information
  • Department of Medical Biochemistry, Faculty of Medicine, Mansoura University, Egypt

  • Department of Rheumatology and Rehabilitation, Faculty of Medicine, Mansoura University, Egypt

  • Sections