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Cytokine- and T Helper-Dependent Lung Mucosal Immunity in Mice with Invasive Pulmonary Aspergillosis

Elio Cenci, Antonella Mencacci, Cristiana Fè d'Ostiani, Giuseppe Del Sero, Paolo Mosci, Claudia Montagnoli, Angela Bacci and Luigina Romani
The Journal of Infectious Diseases
Vol. 178, No. 6 (Dec., 1998), pp. 1750-1760
Published by: Oxford University Press
Stable URL: http://www.jstor.org/stable/30111480
Page Count: 11
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Cytokine- and T Helper-Dependent Lung Mucosal Immunity in Mice with Invasive Pulmonary Aspergillosis
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Abstract

The role of cytokine-and T helper (Th)-dependent lung mucosal antifungal immunity in murine invasive pulmonary aspergillosis (IPA) was investigated. Intact or leukopenic DBA/2 mice were resistant or highly susceptible, respectively, to infection caused by multiple intranasal injections of viable Aspergillus fumigatus conidia. Resistance was associated with unimpaired innate antifungal activity of pulmonary phagocytic cells, concomitant with highlevel production of tumor necrosis factor (TNF)-α and interleukin (IL)-12 and the presence of interstitial lymphocytes producing interferon-γ and IL-2. Conversely, production of TNF-α and IL-12 was down-regulated in highly susceptible mice, which also had defective innate antifungal immunity and high-level production of IL-4 and IL-10 by lung lymphocytes. Resistance was increased in susceptible mice upon local IL-4 or IL-10 neutralization or IL-12 administration. These results indicate that, similar to observations in mice with disseminated aspergillosis, innate and Thl-dependent immunity play an essential role in host defense against IPA.

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