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*
Division of Infectious Diseases, Department of Medicine, University of Cincinnati College of Medicine, Cincinnati, OH 45267; and
Veterans Affairs Hospital, Cincinnati, OH 45220
We examined the influence of endogenous GM-CSF on the course of
primary and secondary pulmonary histoplasmosis. A high proportion
(
75%) of C57BL/6 mice given mAb to GM-CSF did not survive primary
infection, whereas 88–94% of infected controls survived. Analysis of
leukocytes revealed significantly fewer CD4+ and
CD8+ cells in lungs, but not airways, of
anti-GM-CSF-treated mice as compared with infected controls.
However, the histopathology was similar between the two groups. Lungs
of mice given mAb to GM-CSF manifested depressed levels of TNF-
,
IFN-
, and reactive nitrogen intermediates and elevated levels of
IL-4 and IL-10. Administration of mAb to IL-4, to IL-10, or both
restored protective immunity in GM-CSF-neutralized mice. In secondary
infection, administration of mAb to GM-CSF exacerbated infection but
did not alter survival over 30 days. The character of the inflammatory
response was similar, and no differences were detected in Th1 or Th2
cytokine production between the two groups. Thus, endogenous GM-CSF is
essential for survival in primary but not secondary infection, and
blockade perturbs protective immunity. These findings reveal a new
mechanism whereby GM-CSF contributes to host protection and demonstrate
differences in control of primary and secondary
histoplasmosis.
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