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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 (TNF70–80) 3
days before, but not concomitant with, the administration of
Aspergillus conidia resulted in improved survival from
9% in control mice to 55% in TNF70–80-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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H. Briscoe, D. R. Roach, N. Meadows, D. Rathjen, and W. J. Britton A novel tumor necrosis factor (TNF) mimetic peptide prevents recrudescence of Mycobacterium bovis bacillus Calmette-Guerin (BCG) infection in CD4+ T cell-depleted mice J. Leukoc. Biol., October 1, 2000; 68(4): 538 - 544. [Abstract] [Full Text]
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K. Blease, B. Mehrad, T. J. Standiford, N. W. Lukacs, J. Gosling, L. Boring, I. F. Charo, S. L. Kunkel, and C. M. Hogaboam Enhanced Pulmonary Allergic Responses to Aspergillus in CCR2-/- Mice J. Immunol., September 1, 2000; 165(5): 2603 - 2611. [Abstract] [Full Text] [PDF]
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K. Blease, B. Mehrad, T. J. Standiford, N. W. Lukacs, S. L. Kunkel, S. W. Chensue, B. Lu, C. J. Gerard, and C. M. Hogaboam Airway Remodeling Is Absent in CCR1-/- Mice During Chronic Fungal Allergic Airway Disease J. Immunol., August 1, 2000; 165(3): 1564 - 1572. [Abstract] [Full Text] [PDF]
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B. Mehrad, T. A. Moore, and T. J. Standiford Macrophage Inflammatory Protein-1{alpha} Is a Critical Mediator of Host Defense Against Invasive Pulmonary Aspergillosis in Neutropenic Hosts J. Immunol., July 15, 2000; 165(2): 962 - 968. [Abstract] [Full Text] [PDF]
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E. Cenci, A. Mencacci, A. Bacci, F. Bistoni, V. P. Kurup, and L. Romani T Cell Vaccination in Mice with Invasive Pulmonary Aspergillosis J. Immunol., July 1, 2000; 165(1): 381 - 388. [Abstract] [Full Text] [PDF]
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C. M. Hogaboam, K. Blease, B. Mehrad, M. L. Steinhauser, T. J. Standiford, S. L. Kunkel, and N. W. Lukacs Chronic Airway Hyperreactivity, Goblet Cell Hyperplasia, and Peribronchial Fibrosis during Allergic Airway Disease Induced by Aspergillus fumigatus Am. J. Pathol., February 1, 2000; 156(2): 723 - 732. [Abstract] [Full Text] [PDF]
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B. Mehrad, R. M. Strieter, T. A. Moore, W. C. Tsai, S. A. Lira, and T. J. Standiford CXC Chemokine Receptor-2 Ligands Are Necessary Components of Neutrophil-Mediated Host Defense in Invasive Pulmonary Aspergillosis J. Immunol., December 1, 1999; 163(11): 6086 - 6094. [Abstract] [Full Text] [PDF]
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