Abstract
Cytokines are critical molecules necessary for normal lung pathogen host defences. Gamma interferon (IFN-γ) and T1-phenotype immune responses are important components of host defence against Aspergillus. Therefore, we hypothesized that transient overexpression of IFN-γ within the lung could augment host immunity against Aspergillus. Here it was showed that intranasal administration of 5 × 107 colony-forming units (CFU) of Aspergillus fumigatus (Af) induced the expression of IFN-γ. Mice were intranasally (i.n) administrated with 5 × 108 PFU of a recombinant adenovirus vector containing the murine IFN-γ cDNA (AdmIFN-γ), and challenged 24 h later with Af. We observed that i.n. administration of AdmIFN-γ resulted in about a fourfold increase in levels of IFN-γ and IL-12 within the lung, about a 75% reduction in lung fungal contents at day 2 and a more than threefold higher survival rate in the AdmIFN-γ-treated group compared to the controls (P < 001). This protection effect was not found when AdmIFN-γ was i.p. administrated. Alveolar macrophages and lung leucocytes isolated from i.n. AdmIFN-γ- treated animals displayed enhanced killing of intracellular Aspergillus organisms ex vivo. These results demonstrate that transient overexpression of IFN-γ could augment host defence against Aspergillus.
Original language | English (US) |
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Pages (from-to) | 233-241 |
Number of pages | 9 |
Journal | Clinical and Experimental Immunology |
Volume | 142 |
Issue number | 2 |
DOIs | |
State | Published - Nov 2005 |
Externally published | Yes |
Keywords
- Adenovirus
- Fungi
- Gene therapy
- Interferon γ
- Invasive pulmonary aspergillosis
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology