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Lymphotoxin- Double Knockout Mice to Systemic Candidiasis Through Impaired Recruitment of Neutrophils and Phagocytosis of Candida albicans
Departments of
*
Medicine and
Medical Microbiology, University Hospital Nijmegen, Nijmegen, The Netherlands; and
Laboratoire d’Étude des Mécanismes de la Régulation de la Recombinaison Génétique, Unite Mixte de Recherche, Commissariat a l’Energie Atomique/Centre National de la Recherche Scientifique, Fontenay aux Roses, France
TNF-
and lymphotoxin- (LT) are members of the TNF family, and
these cytokines play crucial roles in the defense against infection
with Candida albicans. The aim of the present study was
to investigate the role of endogenous TNF and LT during disseminated
candidiasis in TNF-/-LT-/- knockout mice.
The TNF- and LT-deficient animals had a significantly increased
mortality following C. albicans infection compared with
control mice, and this was due to a 10- to 1000-fold increased
outgrowth of the yeast in their organs. No differences between
TNF-/-LT-/- mice and
TNF+/+LT+/+ were observed when mice were
rendered neutropenic, suggesting that activation of neutrophils
mediates the beneficial effects of endogenous TNF and LT.
Histopathology of the organs, combined with neutrophil recruitment
experiments, showed a dramatic delay in the neutrophil recruitment at
the sites of Candida infection in the
TNF-/-LT-/- mice. Moreover, the neutrophils
of deficient animals were less potent to phagocytize
Candida blastospores than control neutrophils. In
contrast, the killing of Candida and the oxygen radical
production did not differ between neutrophils of
TNF-/-LT-/- and
TNF+/+LT+/+ mice. Peak circulating IL-6 was
significantly higher in TNF-/-LT-/- mice
during infection. Peritoneal macrophages of
TNF-/-LT-/- mice did not produce TNF, and
synthesized significantly lower amounts of IL-1, IL-1
, IL-6, and
macrophage-inflammatory protein-1 than macrophages of
TNF+/+LT+/+ animals did. In conclusion,
endogenous TNF and/or LT contribute to host resistance to disseminated
candidiasis, and their absence in
TNF-/-LT-/- mice renders the animals
susceptible through impaired recruitment of neutrophils and impaired
phagocytosis of C. albicans.
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