Abstracts (complete list) - Wissenschaft Online

Stefanie Kunz, Karin Oberle, Anna Sander, Christian Bogdan, Ulrike Schleicher
Bartonella-Induced Cat Scratch Disease-like
Lymphadenopathy in Mice Involves Cell Proliferation and
Altered Lymphocyte Recruitment
In immunocompetent humans the Gram-negative bacterium Bartonella (B.) henselae,
which has a feline reservoir host and is known as facultative intracellular pathogen,
causes cat scratch disease (CSD). The clinical manifestations of CSD are characterized
by a long-lasting, but self-healing enlargement of the draining lymph node which rarely
contains cultivable Bartonella. So far, no data about the immunopathogenic mechanism
leading to this lymphadenopathy exist.
This prompted us to establish a mouse model of CSD. After subcutaneous infection with
a high dose of B. henselae the bacteria were rapidly eliminated, but similar to human
CSD, a striking and long-lasting swelling of the draining lymph node developed. It was
more severe compared to that induced by other Bartonella species. In vivo-proliferation
assays using 5-Bromo-2`-deoxyuridine (BrdU) and the transfer of
carboxyfluoresceinsuccinimidylester (CFSE)-labeled splenocytes revealed that cell
proliferation and a preferential influx of B cells contributed to the observed lymph node
enlargement after Bartonella infection. With respect to possible immunostimulatory
functions of Bartonella, we found that plasmacytoid dendritic cells exposed to Bartonella
in vitro secreted high amounts of interferon (IFN)-α/β. Compared to B. henselae, the
rodent pathogen B. grahamii elicited only a mild lymph node swelling in wildtype mice,
but a severe lymphadenopathy in IFN-α/β receptor-deficient mice. From these data, we
conclude that lymphoproliferation as well as altered immune cell recruitment are
involved in the pathogenesis of B. henselae-induced lymphadenopathy in mice.
Furthermore our data suggest an inhibitory effect of IFN-α/β on the described
lymphadenopathy in mice.