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,
*
Department of Microbiology and Immunology and
University of Massachusetts Medical School, Worcester, MA 01605; and Departments of
Pathology and
Medicine, Division of Infectious Diseases, Albert Einstein College of Medicine, Bronx, NY 10461
We investigated the pathogenesis of pulmonary Cryptococcus
neoformans infection and passive Ab efficacy in mice deficient
in inducible NO synthase (NOS2-/-) and the
parental strain. Parental mice lived significantly longer than
NOS2-/- mice after intratracheal infection, despite
having a higher lung fungal burden. Administration of Ab reduced lung
CFU in both NOS2-/- and parental mice, but prolonged
survival and increased the inflammatory response only in parental mice.
Ab administration was associated with increased serum nitrite and
reduced polysaccharide levels in parental mice. Eosinophils were
present in greater numbers in the lung of infected
NOS2-/- mice than parental mice, irrespective of Ab
administration. C. neoformans infection in
NOS2-/- mice resulted in significantly higher levels of
IFN-
, monocyte chemoattractant protein-1, and
macrophage-inflammatory protein-1
than parental mice. Ab
administration had different effects on infected NOS2-/-
and parental mice with respect to IFN-, monocoyte chemoattractant
protein-1, and macrophage-inflammatory protein-1 levels. Ab
administration increased lung levels of IFN- in parental mice and
reduced levels in NOS2-/- mice. The results indicate that
NO is involved in the regulation of cytokine expression in response to
cryptococcal pneumonia and is necessary for Ab efficacy against
C. neoformans in mice. Our findings indicate a complex
relationship between Ab efficacy against C. neoformans
and cytokine expression, underscoring the interdependency of cellular
and humoral defense mechanisms.
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