Innate immunity to Aspergillus species

Abstract

All humans are continuously exposed to inhaled Aspergillus conidia, yet healthy hosts clear the organism without developing disease and without the development of antibody- or cell-mediated acquired immunity to this organism. This suggests that for most healthy humans, innate immunity is sufficient to clear the organism. A failure of these defenses results in a uniquely diverse set of illnesses caused by Aspergillus species, which includes diseases caused by the colonization of the respiratory tract, invasive infection, and hypersensitivity. A key concept in immune responses to Aspergillus species is that the susceptibilities of the host determine the morphological form, antigenic structure, and physical location of the fungus. In this review, we summarize the current literature on the multiple layers of innate defenses against Aspergillus species that dictate the outcome of this host-microbe interaction.

FIG. 1.

Diagrammatic representation of diseases attributed to Aspergillus species as a function of the host's immune response. ABPA, allergic bronchopulmonary aspergillosis.

FIG. 2.

Schematic representation of components of the host response to inhaled Aspergillus conidia. PMN, polymorphonuclear leukocytes.

FIG. 3.

Association of Aspergillus species with bronchial epithelial cells in vivo. Shown is representative lung histology from neutropenic mice 3 days after intratracheal challenge with a sublethal inoculum of Aspergillus conidia, with sequential sections stained with hematoxylin and eosin to show mammalian cell morphology (A and C) and Grocott's methenamine silver to demonstrate fungal elements (B and D). (A and B) Extensive association of fungal elements with airway lining. (C and D) Higher-power images of the boxed areas in A and B showing that most of the fungal material appears to be intracellular. All scale bars are 20 μm; original magnifications, ×100 (A and B) and ×400 (C and D).