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ECPB 2019, 87(3): 44–50
Research articles

Peculiarities of lymphocytic pool in the blood of reactive arthritis patients with Epstein-Barr viral and chlamydial infections in the background


Reactive arthritis is an immune inflammatory joint disease that occurs after a bacterial or viral infection and it is a systemic manifestation of these infections. The peculiarity of reactive arthritis pathogenesis is the persistence of intracellular pathogens in the patient's body.

Currently, special attention is paid to the role of herpesvirus infection, primarily Epstein-Barr virus (EВV) in the development of reactive arthritis. EBV replicates primarily in immunocompetent cells, particularly B-lymphocytes and epithelial cells. Therefore, the aim of this study was to identify the condition of the lymphocytic pool in patients with reactive arthritis caused by chlamydia and EBV infection. Verification of reactive arthritis was conducted based on clinical data on affected joints, laboratory and instrumental studies. Patients with reactive arthritis met the diagnostic criteria according to the Protocol of the Ministry of Health Care of Ukraine as of October 12, 2016. Bacteriological examination of throat cultures to identify the probable infection with the bacterial pathogens that usually cause tonsillitis (Streptococcus, Staphylococcus) was performed in all patients. EBV infection was verified by clinical and laboratory, serological (identification of specific IgM, IgG to various EBV antigens), and molecular genetic (detection of DNA virus) studies. To diagnose Chlamydia infection, the presence of specific antibodies IgM, IgG, IgA to C. trachomatis and DNA bacteria were investigated.

Lymphocyte phenotyping and determination of the expression of the main activation markers was conducted with flow cytofluorometry technique using appropriate BD Multitest monoclonal antibodies of Bekton Dickenson (USA). Our results indicate quantitative changes in the functional characteristics of peripheral blood lymphocytes in patients with reactive arthritis.

There was a significant (P<0.05) increase in the absolute number of CD 45-lymphocytes (g/L) in patients with EBV (2.62±0.35 g/L; P<0.05) and in patients with double infection - EBV and C. Trachomatis (2.43±0.27 g/L; P<0.05) compared with patients with reactive arthritis induced by tonsillitis (1.83±0.23 g/L). The relative number of T-cytotoxic (CD8+) lymphocytes decreased compared to healthy individuals in three trial groups: reactive arthritis and C. Trachomatis (22±4.9%), reactive arthritis with double infection - EBV and C. Trachomatis (21±6.8%), reactive arthritis and EBV. The absolute number of T-helpers was significantly higher in patients with reactive arthritis and double infection - EBV and C. Trachomatis (0.96±0.06 g/L) and reactive arthritis and EBV (0.91±0.05 g/L) compared to healthy individuals (0.70±0.05 g/L, P<0.05). An increase in the number of T-helpers in patients with reactive arthritis may indicate a powerful stimulating activity of these infections on the lymphocytes of patients. A significant increase in the subpopulation of B-lymphocytes (CD3-CD19+) in relative and absolute values in patients with reactive arthritis and EBV (20±4.5%, 0.36±0.031 g/L) compared with healthy individuals (15±4.2%, 0.23±0.027 g/L, P<0.05) was observed. It is known that the virus can act as an adjuvant in the development of autoimmunity, stimulating the immune response nonspecifically, disrupting immunological control over EBV replication. Chlamydia as intracellular organisms are also able to avoid specific immune cleansing, which is the ground for the persistence of antigens. Thus, the long-term persistence of microbial components of chlamydia and EBV contributes to joint damage, increases lymphocytic expansion, strengthens the systemic immune response, which can lead to autoimmunization, and further cause the development of rheumatoid arthritis.

Received: 30.08.2019

Keywords: Reactive arthritis, Epstein-Barr virus, Chlamidia Trachomatis, autoimmune diseases

Full text: PDF (Ukr) 363K

  1. 1. Zhuravleva MO. Evaluation of the effectiveness and tolerability of azithromycin (sumamed) courses of various durations for urogenic reactive arthritis. Revmatologija. 2014;3:31-5). [in Russian].
  2. 2. Spaska GO. Reactive Arthritis: a modern look at the problem. Ukrainian Medical Journal 2011;6(86):42-4). [in Ukrainian].
  3. 3. Boyko YE. Reactive arthritis is most often a rheumatologic disease of childhood. Dytyachyy likar. 2009;1:25-8). [in Ukrainian].
  4. 4. Soroka NF. Rheumatoid arthritis associated with chlamydial infection. Zdravohraneniye. 2009;1:4-9). [in Russian].
  5. 5. Ostaszewska-Puchalska I, Zdrodowska-Stefanow B, Kuryliszyn-Moskal A, Bułhak-Kozioł V, Sokołowska M. Incidence of Chlamydia trachomatis infection in patients with reactive arthritis. Reumatologia. 2015;53(2):69-73.
  6. 6. Jassim NS, Aboud RS, Joda AT, Fadil HY, Humadani FG, Ahmed DM et al. Detection of Epstein-Barr virus Capsid antigen (EBV CA) in Sera of Rheumatoid Arthritis, Reactive Arthritis and Ankylosing Spondylitis Patients. Iraqi Journal of Science. 2015;56(4B):3130-34.
  7. 7. Draborg AH. Duus K, Houen G. Epstein-Barr Virus in Systemic Autoimmune Diseases. Clinical and Developmental Immunology. 2013;23:21-9.
  8. 8. Martorelli D, Muraro E, Merlo A, Turrini R, Fae D-A, Rosato A et al. Exploiting the Interplay between Innate and Adaptive Immunity to Improve Immunotherapeutic Strategies for Epstein-Barr-Virus-Driven Disorders. Clinical and Developmental Immunology. 2012;6:1155-73.
  9. 9. Moradi B, Schnatzer Ph, Hagmann S, Rosshirt N, Gotterbarm T, Kretzer J et al. CD4+CD25+/highCD127low/- regulatory T cells are enriched in rheumatoid arthritis and osteoarthritis joints - analysis of frequency and phenotype in synovial membrane, synovial fluid and peripheral blood. Arthritis Research & Therapy. 2014;
  10. 10. Costenbader KH, Karlson EW. Epstein-Barr virus and rheumatoid arthritis: is there a link? Arthritis Research & Therapy. 2006;8(1):204-10.
  11. 11. Hamdulay SS, Glynne SJ, Keat A. When is arthritis reactive? Postgrad Med J. 2006;82:446-53.
  12. 12. Chopyak VV, Potemkina GA, Zubchenko SA. Monitoring the effectiveness of the use of groprinosin based on the analysis of TLR9 expression on immunocompetent cells in the treatment of chronic Epstein-Barr virus infection in the stage of replicative activity. Oraldyn Gylym Zharshysy. 2014;86(7):69-77). [in Russion].
  13. 13. Amital H, Govoni M, Maya R, Meroni PL, Ori B, Shoenfeld Y et al. Role of infectious agents in systemic rheumatic diseases. Clinical and experimental rheumatology. 2008;1:27-32.
  14. 14. Fujiwara S, Takei M. Epstein-Barr virus and autoimmune diseases. Clinical and Experimental Neuroimmunology. 2015;6(1):38-48.
  15. 15. Arleevskaya MI, Kravtsova OA, Tsibulkin AP, Lemerle J, Renaudineau Y. How Herpesviridae Combined with other Viral Infections can Trigger and Drive Rheumatoid Arthritis. Lupus Open Access. 2016;1(2):102-4.

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