Effect of Infliximab on IFN-γ and IL-4 Expression in Peripheral Blood and Inflamed Intestinal Mucosa of Patients with Crohn’s Disease
Ivan Ferkolj¹*, Saša Marković¹, @eljka Većerić¹, Alojz Ihan², Maja Pohar³
¹ University Medical Centre Ljubljana, Division of Internal Medicine,
Department of Gastroenterology, Ljubljana, Slovenia
² Institute of Microbiology and Immunology, Faculty of Medicine, University of
Ljubljana, Slovenia
³ Institute of Biomedical Informatics, Faculty of Medicine, University of
Ljubljana, Slovenia
Tel: +386 41 519879,
Fax: +386 1 4334190,
E-mail: ivan.ferkolj@kclj.si
Abstract
Background: Infliximab, a monoclonal anti-tumor necrosis factor alpha (TNF-α)
antibody, is an effective treatment for Crohn’s disease without prior
response to conventional therapy. It binds with high affinity to soluble and
membranebound TNF-α, neutralizing its biological activity and reducing TNF-α
production by mucosal cells. Its influence on other cytokines has been
investigated to a much smaller extent. Aim: The aim of the study was to
establish the influence of infliximab on cells containing the proinflammatory
cytokine interferon-gamma (IFN-γ) and the anti-inflammatory cytokine interleukin-4
(IL-4) in peripheral blood and inflamed intestinal mucosa. Methods: Twenty-five
patients with Crohn’s disease (11 with the luminal and 14 with the fistular
form) underwent treatment with infliximab. IFN-γ and IL- 4 containing cells in
peripheral blood and inflamed intestinal mucosa were analysed by flow cytometry
before and 14 days after the treatment. Results: Twenty-two patients (88%)
showed a clinical response to the drug and three (12%) had no response. In the
group of responders, the proportion of cells containing IFN-γ and IL-4 in
peripheral blood and inflamed intestinal mucosa remained unchanged after the
treatment. Conclusions: Infliximab has no direct influence on cells containing
IFN-γ and IL-4 in peripheral blood and inflamed intestinal mucosa. The
insignificant changes in the proportions of these cells observed after the
treatment may be attributed to its direct effect on TNF-α, which resulted in
silencing of the inflammation.
Keywords: Crohn’s disease, infliximab, interferon-gamma, interleukin-4