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Exacerbates Primary and Secondary Pulmonary Histoplasmosis by Differential Mechanisms1
Division of Infectious Diseases, University of Cincinnati College of Medicine, Cincinnati, OH 45267, and Cincinnati Veterans Affairs Medical Center, Cincinnati, OH 45220
We investigated the mechanisms by which endogenous TNF-
modulates host defenses during experimental primary and secondary
pulmonary infection with Histoplasma capsulatum (Hc).
Neutralization of TNF- in vivo resulted in increased CFU and 100%
mortality in naive and immune mice challenged with Hc intranasally.
Levels of IFN-
and granulocyte macrophage-CSF were elevated in
TNF--neutralized naive mice, whereas IL-4, -6, -10 and TGF-ß did
not differ from controls. In contrast, in secondary histoplasmosis,
significant elevations of IL-4 and -10 were observed in
TNF--depleted mice. Alveolar macrophages (M
) did not exert
fungistatic activity against Hc after exposure to recombinant murine
TNF-, recombinant murine IFN-, or both. The increase in
susceptibility to primary Hc infection was associated with diminished
production of reactive nitrogen intermediates by alveolar M from
TNF--depleted mice, whereas production of nitric oxide during
secondary histoplasmosis was similar in both groups. Upon secondary
challenge, TNF--depleted mice were rescued by concomitant
neutralization of IL-4 and IL-10, but not either cytokine alone. Thus,
TNF- is critical for controlling primary and secondary infection
with Hc, and the mechanisms that lead mice to succumb to primary or
secondary infection when endogenous TNF- is blocked are different.
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