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Egyptian Rheumatology and Rehabilitation
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Study of plasma levels of soluble triggering receptor expressed on myeloid cells-1 in rheumatoid arthritis and its correlation with disease activity and tumor necrosis factor-α

Egyptian Rheumatology and Rehabilitation volume 45, pages 18–24 (2018)Cite this article

Abstract

Aim of the work

The triggering receptor expressed on myeloid cells-1 (TREM-1) is a cell surface receptor expressed mainly on monocytes and neutrophils. It acts as an amplifier of inflammatory response in acute and chronic inflammatory states. The aim of this work was to study the plasma-soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) in rheumatoid arthritis (RA) patients and its correlation with disease activity and tumor necrosis factor-α (TNF-α).

Patients and methods

This study included 80 patients with RA and 20 age-matched and sex-matched controls. All were subjected to demographic, clinical, laboratory, and radiological studies using the 28-joint Disease Activity Score, erythrocyte sedimentation rate, complete blood count, and radiograph of both hands. Plasma levels of sTREM-1 and TNF-α were measured with enzyme-linked immunosorbent assay.

Results

RA patients had significantly higher sTREM-1 and TNF-a levels compared with controls (206.32±125.75 and 17.83±11.88; P<0.001) and (190.82±69.46 and 54.75±9.46; P<0.001). In RA patients, sTREM-1 levels were found to be positively correlated with 28-joint Disease Activity Score, erythrocyte sedimentation rate, and TNF-a level (r=0.408, P=0.001; r=0.287, P=0.010; r=0.749, P=0.001). sTREM-1 level was significantly increasing as patients had increasing disease activity (F-test=20.62; P=0.001).

Conclusion

RA patients had higher sTREM-1 and TNF-a level compared with controls, and sTREM-1 level was correlated with disease activity, suggesting that sTREM-1 plays a role in the inflammatory process associated with TNF-a, and it may be a useful disease activity marker in RA. TREM-1 may be a safe therapeutic strategy for RA, as blocking TREM-1 signaling was found to suppress inflammatory responses without affecting the immune system to fight bacterial infection.

References

  1. Scott DL, Wolfe F, Huizinga TW. Rheumatoid arthritis. Lancet 2010; 376:1094–1108.

    Article  Google Scholar 

  2. El Bakry Samah A, Bassyouni IH, Reem El-Shazly B, Abou-El Alla AA. Clinical significance of soluble-triggering receptor expressed on myeloid cells-1 (sTREM-1) in patients with rheumatoid arthritis. Egypt Rheumatol 2013; 35:95–100.

    Article  Google Scholar 

  3. Derive M, Massin F, Gibot S. Triggering receptor expressed on myeloid cells-1 as a new therapeutic target during inflammatory diseases. Self Nonself 2010; 1:225–230.

    Article  Google Scholar 

  4. Tessarz AS, Cerwenka A. The TREM-1/DAP12 pathway. Immunol Lett 2008; 116:111–116.

    Article  CAS  Google Scholar 

  5. Sung JC, Tae H-K., Young HL, Gwan GS, Jong DJ. Levels of plasma-soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) are correlated with disease activity in rheumatoid arthritis. J Rheumatol 2012; 39:933–938.

    Article  Google Scholar 

  6. Kuai J, Gregory B, Hill A, Pittman DD, Feldman JL, Brown T, et al. TREM-1 expression is increased in the synovium of rheumatoid arthritis patients and induces the expression of pro-inflammatory cytokines. Rheumatology (Oxford) 2009; 48:1352–1358.

    Article  CAS  Google Scholar 

  7. Collins CE, La DT, Yang HT, Massin F, Gibot S, Faure G, et al. Elevated synovial expression of triggering receptor expressed on myeloid cells 1 in patients with septic arthritis or rheumatoid arthritis. Ann Rheum Dis 2009; 68:1768–1774.

    Article  CAS  Google Scholar 

  8. Aletaha D, Neogi T, Silman AJ, Funovits J, Felson DT, Bingham 3rd CO, et al. Rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Arthritis Rheum 2010; 62: 2569–2581.

    Article  Google Scholar 

  9. Prevoo ML, van’t Hof MA, Kuper HH, van Leeuwen MA. Modified disease activity scores that include twenty-eight-joint counts: development and validation in a prospective longitudinal study of patients with rheumatoid arthritis. Arthritis Rheum 1995; 38:44–48.

    Article  CAS  Google Scholar 

  10. Westergren A. Determination of erythrocyte sedimentation rate. Ann Med 1924; 26:577.

    Google Scholar 

  11. Wolfe F, Cathey MA, Roberts FK. The latex test revisited: rheumatoid factor testing in 8287 rheumatic disease patients. Arthritis Rheum 1991; 34:951–960.

    Article  CAS  Google Scholar 

  12. Van Gaalen FA, Linn-Rasker SP, van Venrooij WJ. Autoantibodies to cyclic citrullinated peptides predict progression to rheumatoid arthritis in patients with undifferentiated arthritis: a prospective cohort study. Arthritis Rheum 2004; 50:709–715.

    Article  Google Scholar 

  13. Leroy JLC, Leory OPR. Evaluation of a rapid slide latex agglutination assay for the qualitative and semi-quantitative determination of C-reactive protein (CRP) in human serum: Adv Diag Test 1995; 10:1.

  14. Bouchon A, Dietrich J, Colonna M. Cutting edge: inflammatory responses can be triggered byTREM-1, a novel receptor expressed on neutrophils and monocytes. J Immunol 2000; 164:4991–4995.

    Article  CAS  Google Scholar 

  15. Beutler B, Greenwald D, Hulmes JD. Identity of tumour necrosis factor and the macrophage-secreted factor cachectin. J Immunol 1985; 170:1812–1818.

    Google Scholar 

  16. Brennan FM, McInnes IB. Evidence that cytokines play a role in rheumatoid arthritis. J Clin Invest 2008; 118:3537–3545.

    Article  CAS  Google Scholar 

  17. Choy E. Understanding the dynamics: pathways involved in the pathogenesis of rheumatoid arthritis. Rheumatology (Oxford) 2012; 51 (Suppl 5):v3-v11.

  18. Caporali R, Pallavicini FB, Filippini M, Gorla R, Marchesoni A, Favalli EG, et al. Treatment of rheumatoid arthritis with anti TNF alpha agents: a reappraisal. Autoimmun Rev 2009; 8:274–280.

    Article  CAS  Google Scholar 

  19. Murakami Y, Akahoshi T, Aoki N, Toyomoto M, Miyasaka N, Kohsaka H. Intervention of an inflammation amplifier, triggering receptor expressed on myeloid cells 1, for treatment of autoimmune arthritis. Arthritis Rheum 2009; 60:1615–1623.

    Article  CAS  Google Scholar 

  20. Iwai H, Kohsaka H. Blockade of triggering receptor expressed on myeloid cells-1 as a new therapy of arthritis. Nihon Rinsho Meneki Gakkai Kaishi 2012; 35:81–86.

    Article  CAS  Google Scholar 

  21. Bleharski JR, Kiessler V, Buonsanti C, Sieling PA, Stenger S, Colonna M, et al. A role for triggering receptor expressed on myeloid cells-1 in host defense during the early-induced and adaptive phases of the immune response. J Immunol 2003; 170: 3812–3818.

    Article  CAS  Google Scholar 

  22. Hochberg MC, Arnold CM, Hogans BB, Spivak JL. Serum immunoreactive erythropoietin in rheumatoid arthritis: impaired response to anemia. Arthritis Rheum 1988; 31:1318–1321.

    Article  CAS  Google Scholar 

  23. Means RT Jr, Krantz SB. Inhibition of human erythroid colony-forming units by tumor necrosis factor require beta interferon. J Clin Invest 1993; 91:416–419.

    Article  CAS  Google Scholar 

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Authors and Affiliations

  1. Department of Physical Medicine, Rheumatology and Rehabilitation, Faculty of Medicine, Zagazig University, Zagazig, Egypt

    Abd El-Samed I. El-Hewala

  2. Department of Physical Medicine, Rheumatology and Rehabilitation, Menoufia, Egypt

    Samar G. Soliman, Heba A. Esaily & Eman A. Abd Allah MD

  3. Department of Clinical Biochemstry, Faculty of Medicine, Menoufia University, Menoufia, Egypt

    Eman Badr

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  1. Abd El-Samed I. El-Hewala
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  2. Samar G. Soliman
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  4. Heba A. Esaily
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  5. Eman A. Abd Allah MD
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Correspondence to Eman A. Abd Allah MD.

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El-Hewala, A.ES.I., Soliman, S.G., Badr, E. et al. Study of plasma levels of soluble triggering receptor expressed on myeloid cells-1 in rheumatoid arthritis and its correlation with disease activity and tumor necrosis factor-α. Egypt Rheumatol Rehabil 45, 18–24 (2018). https://doi.org/10.4103/1110-161X.222634

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  • DOI: https://doi.org/10.4103/1110-161X.222634

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