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Production, Imparting Pathogenicity on Blastomyces dermatitidis1
,
,§
Departments of
*
Pediatrics,
Internal Medicine, and
Medical Microbiology and Immunology, and
§
Comprehensive Cancer Center, University of Wisconsin Medical School, University of Wisconsin Hospital and Clinics, Madison, WI
The WI-1 adhesin is indispensable for pathogenicity of
Blastomyces dermatitidis and is thought to promote
pulmonary infection by fixing yeast to lung tissue and cells. Recent
findings suggest that WI-1 confers pathogenicity by mechanisms in
addition to adherence. Here, we investigated whether WI-1 modulates
host immunity by altering production of pro-inflammatory cytokines.
Production of TNF-
in lung alveolar fluids of mice infected with
B. dermatitidis was severalfold higher for WI-1 knockout
yeast compared with wild-type yeast, and in vitro coculture of
unseparated lung cells with these isogenic yeast disclosed similar
differences. Upon coculture with purified macrophages and neutrophils,
wild-type yeast blocked TNF- production, yet WI-1 knockout yeast
stimulated production. Coating knockout yeast with purified WI-1
converted them from stimulating TNF- production to inhibiting
production. Addition of purified WI-1 into stimulated phagocyte
cultures led to concentration-dependent inhibition of TNF-
production. Neutralization of TNF- in vivo exacerbated experimental
pulmonary infection, particularly for the nonpathogenic WI-1 knockout
yeast. Inducing increased TNF- levels in the lung by
adenovirus-vectored gene therapy controlled infection with wild-type
yeast. Thus, the WI-1 adhesin on yeast modulates host immunity through
blocking TNF- production by phagocytes, which fosters progression of
pulmonary infection.
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