Systemic suppression of interferon- responses in Buruli ulcer patients resolves after surgical excision of the lesions caused by the extracellular pathogen Mycobacterium ulcerans
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Date
2006
Journal Title
Journal ISSN
Volume Title
Publisher
Journal of Leukocyte Biology
Abstract
Buruli ulcer (BU), caused by Mycobacterium
ulcerans, is the third most common mycobacterial
infection in immunocompetent humans
besides tuberculosis and leprosy. We have compared
by ex vivo enzyme-linked immunospot analysis
interferon- (IFN- ) responses in peripheral
blood mononuclear cells (PBMC) from BU patients,
household contacts, and individuals living in
an adjacent M. ulcerans nonendemic region.
PBMC were stimulated with purified protein derivative
(PPD) and nonmycobacterial antigens such as
reconstituted influenza virus particles and isopentenyl-
pyrophosphate. With all three antigens, the
number of IFN- spot-forming units was reduced
significantly in BU patients compared with the controls
from a nonendemic area. This demonstrates
for the first time that M. ulcerans infection-associated
systemic reduction in IFN- responses is not
confined to stimulation with live or dead mycobacteria
and their products but extends to other antigens.
Interleukin (IL)-12 secretion by PPD-stimulated
PBMC was not reduced in BU patients, indicating
that reduction in IFN- responses was not
caused by diminished IL-12 production.Several
months after surgical excision of BU lesions,
IFN- responses of BU patients against all antigens
used for stimulation recovered significantly,
indicating that the measured systemic immunosuppression
was not the consequence of a genetic
defect in T cell function predisposing for BU but
is rather related to the presence of M. ulcerans
bacteria. J. Leukoc. Biol. 79: 1150–1156;
2006.
Description
Research Article
Keywords
ex vivo ELISpot analysis, immunosuppression, interleukin- 12