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in Pulmonary Host Defense in Murine Invasive Aspergillosis1
Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of Michigan Medical School, Ann Arbor, MI 48109
Invasive pulmonary aspergillosis is a common and devastating
complication of immunosuppression, whose incidence has increased
dramatically in tandem with the increase in the number of
immunocompromised patients. Given the role of TNF-
in other
pulmonary infections, we hypothesized that TNF-
is an important
proximal signal in murine invasive pulmonary aspergillosis.
Intratracheal challenge with Aspergillus fumigatus
conidia in both neutropenic (cyclophosphamide-treated) and
nonneutropenic BALB/c mice resulted in the time-dependent increase in
lung TNF-
levels, which correlated with the histologic development
of a patchy, peribronchial infiltration of mononuclear and
polymorphonuclear cells. Ab-mediated neutralization of TNF-
resulted
in an increase in mortality in both normal and cyclophosphamide-treated
animals, which was associated with increased lung fungal burden as
determined by histology and as quantified by chitin content. Depletion
of TNF-
resulted in a reduced lung neutrophil influx in both normal
and cyclophosphamide-treated animals, which occurred in association
with a decrease in lung levels of the C-X-C chemokine, macrophage
inflammatory protein-2 and the C-C chemokines macrophage inflammatory
protein-1
and JE. In cyclophosphamide-treated animals, intratracheal
administration of a TNF-
agonist peptide (TNF7080) 3
days before, but not concomitant with, the administration of
Aspergillus conidia resulted in improved survival from
9% in control mice to 55% in TNF7080-treated animals.
These studies indicate that TNF-
is a critical component of innate
immunity in both immunocompromised and immunocompetent hosts, and that
pretreatment with a TNF-
agonist peptide in a compartmentalized
fashion can significantly enhance resistance to A.
fumigatus in neutropenic animals.
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