Immune response to biological therapy for inflammatory bowel diseases


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Abstract

AIM: To study biological (cell and anticytokine) therapy-induced changes in the levels of proinflammatory cytokines in patients with inflammatory bowel diseases (IBD)/MATERIAL AND METHODS: Forty-four patients with chronic continuous or chronic recurrent IBD were examined. According to the performed therapy, the patients were divided into 3 groups: 1) 16 patients who took infliximab; 2) 14 patients who received combination anti-inflammatory therapy with the cultured mesenchymal stromal cells (MSC) being administered; 3) 14 patients who had standard anti-inflammatory therapy with 5-aminosalycilic acid preparations and glucocorticosteroids. The concentrations of tumor necrosis factor-α (TNF-α), interferon-γ (INF-γ), and interleukins (IL)-2, -5, -8, -12, and -15 were determined in the patients' sera before and 2 months after therapy initiation/RESULTS: The elevation in the serum levels of the proinflammatory cytokines TNF-α, INF-γ, and IL-2, -5, -8, -12, and -15 indicates their implication in the pathogenesis of ulcerative colitis and Crohn's disease. Their levels may evaluate both the activity of an inflammatory process and the efficiency of the therapy. The higher level of these cytokines is accompanied by the enhanced activity of diseases, which may be used to diagnose their activity, to predict the course of IBD, and to perform adequate therapy. The decreased level of the proinflammatory cytokines is indicative of the efficiency of the therapy in patients with IBD/CONCLUSION: By reducing TNF-α levels, infliximab therapy results in a decrease in the concentrations of other proinflammatory cytokines (IL-1, -2, -5, -8), thus lowering the inflammatory activity of IBD. MSC transplantation also reduces the level of most proinflammatory cytokines, thus diminishing the intensity of immunopathological processes, which is shown by positive changes in the clinical picture of the disease.

About the authors

O V Kniazev

Центральный научно-исследовательский институт гастроэнтерологии Департамента здравоохранения Москвы

Email: oleg7@bk.ru

A I Parfenov

Центральный научно-исследовательский институт гастроэнтерологии Департамента здравоохранения Москвы

Email: asfold@mail.ru

I N Ruchkina

Центральный научно-исследовательский институт гастроэнтерологии Департамента здравоохранения Москвы

Email: ruchkinai@mail.ru

L B Lazebnik

Центральный научно-исследовательский институт гастроэнтерологии Департамента здравоохранения Москвы

V É Sagynbaeva

Центральный научно-исследовательский институт гастроэнтерологии Департамента здравоохранения Москвы

Email: venera_32@rambler.ru

References

  1. Sands B.E., Winston B., Salzberg B. et al. Randomized, controlled trial of recombinant human interleukin II in patients with active Crohn's disease. Aliment Pharmacol Ther 2002; 16: 399-406.
  2. Beutler B.A. The role of tumor necrosis factor in health and disease. J Rheumatol 1999; 26 (Suppl. 57): 16-21.
  3. Ahrenstedt O., Knutson L., Nilson B. et al. Enhanced local production of complement components in the small intestines of patients with Crohn's disease. N Engl J Med 1990; 322: 1345-1349.
  4. Rutgeerts P., Feagan B.G., Lichtenstein G.R. et al. Comparison of scheduled and episodic treatment strategies of infliximab in Crohn's disease. Gastroenterology 2004; 126: 402-413.
  5. Eapen M., Rubinstein P., Zhang M.J. et al. Outcomes of transplantation of unrelated donor umbilical cord blood and bone marrow in children with acute leukemia: a comparison study. Lancet 2007; 369: 1947-1954.
  6. Цыб А.Ф., Рошаль Л.М., Южаков В.В. и др. Морфофункциональное изучение терапевтического эффекта аутологичных мезенхимальных стволовых клеток при экспериментальной диффузной травме головного мозга крыс. Клеточн технол в биол и мед 2006; 3: 157-165.
  7. Porada C.D., Zanjani E.D., Almeida-Porad G. Adult mesenchymal stem cells: a pluripotent population with multiple applications. Curr Stem Cell Res Ther 2006; 1 (3): 365-369.
  8. Uccelli A., Pistoia V., Moretta L. Mesenchymal stem cells: a new strategy for immunosuppression? Trends Immunol 2007; 28: 219-226.
  9. Abdi R., Fiorina P., Adra C.N. et al. Immunomodulation by mesenchymal stem cells: a potential therapeutic strategy for type 1 diabetes. Diabetes 2008; 57: 1759-1767.
  10. Corcione A., Benvenuto F., Ferretti E. et al. Human mesenchymal stem cells modulate B-cell functions. Blood 2006; 107: 367-372.
  11. Sotiropoulou P.A., Perez S.A., Gritzapis A.D. et al. Interactions between human mesenchymal stem cells and natural killer cells. Stem Cells 2006; 24 (1): 74-854.
  12. Zhang W., Ge W., Li C. et al. Effects of mesenchymal stem cells on differentiation, maturation, and function of human monocyte-derived dendritic cells. Stem Cells Dev 2004; 13: 263-271.
  13. Baeten D., van Damme N., van den Bosch F. et al. Impaired Th1 cytokine production in spondiloarthropathy is restored by anti-TNF alpha. Ann Rheum Dis 2001; 60: 755-765.
  14. Zou J.X., Rudmaleit M., Brandt J. et al. Down-regulation of non-specific and antigen-specific T cell cytokine response in ankylosing spondilitis during treatment with infliximab. Arthritis Rheum 2003; 48: 780-790.
  15. Фарелл Р., Пепперкорн М. Язвенный колит. Междунар мед журн 2003; 1: 73-80.
  16. Белоусова Е.А., Морозова Н.А., Никитина Н.В. Инфликсимаб (ремикейд) в лечении рефрактерных форм болезни Крона. Рус мед журн 2005; 1: 28-32.
  17. Белоусова Е.А. Биологическая стратегия в лечении воспалительных заболеваний кишечника. Фарматека 2006; 6: 6-10.

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