DECREASED INTERLEUKIN-4 AND INCREASED GAMMA-INTERFERON PRODUCTION BY PERIPHERAL-BLOOD MONONUCLEAR-CELLS OF PATIENTS WITH LYME BORRELIOSIS

Citation
J. Oksi et al., DECREASED INTERLEUKIN-4 AND INCREASED GAMMA-INTERFERON PRODUCTION BY PERIPHERAL-BLOOD MONONUCLEAR-CELLS OF PATIENTS WITH LYME BORRELIOSIS, Infection and immunity, 64(9), 1996, pp. 3620-3623
Citations number
32
Categorie Soggetti
Immunology,"Infectious Diseases
Journal title
ISSN journal
00199567
Volume
64
Issue
9
Year of publication
1996
Pages
3620 - 3623
Database
ISI
SICI code
0019-9567(1996)64:9<3620:DIAIGP>2.0.ZU;2-0
Abstract
Spontaneous and Borrelia burgdorferi-stimulated proliferation of perip heral blood mononuclear cells (PBMCs) and their interleukin-4 (IL-4), gamma interferon (IFN-gamma), and NO production were measured in 36 pa tients with second- or third-stage Lyme borreliosis (LB) and 11 contro l subjects, Spontaneous proliferation of PBMCs was significantly highe r (P = 0.0003) in the LB patients than in the control subjects, Sponta neous production of IL-4 was significantly lower in patients than in c ontrol subjects (P = 0.0007), but spontaneous production of IFN-gamma was slightly higher in patients, The proliferative response of PBMCs t o stimulation with B. burgdorferi was significantly higher (P = 0.01) in patients. The B. burgdorferi-induced production of LFN-gamma (P = 0 .002) was also significantly higher in patients, The spontaneous and B . burgdorferi-induced production of NO showed no significant differenc e between patients and control subjects, These findings indicate that the activation of PBMCs in patients with late LB is enhanced in vivo, Furthermore, the production of IL-4 is effectively suppressed spontane ously, whereas the production of IFN-gamma by PBMCs is slightly increa sed spontaneously and significantly enhanced during stimulation viith B. burgdorferi in vitro, The ''spontaneous'' or disease-induced altera tions in cytokine levels of patients, in this case suppression of a Th 2-type cytokine production and activation of a Th1-type cytokine produ ction, may contribute to the pathogenesis of LB.