Aspergillus fumigatus conidia modulate the endocytic pathway of alveolar macrophages.

Ref ID: 15904

Author:

Andreas Thywissen1, 3, Thorsten Heinekamp1,
Hans-Martin Dahse2, Peter F. Zipfel2, 3, and Axel A. Brakhage1,

Author address:

Leibniz Institute for Natural Product Research and Infection Biology
Hans-Knoell-Institute (HKI), Department of Molecular and Applied Microbiology, Jena, Germany. 2 Leibniz Institute for Natural Product Research and
Infection Biology Hans-Knoel

Full conference title:

26th Fungal Genetics Conference

Date: 15 March 2014

Abstract:

The mould Aspergillus fumigatus is the main causative agent of invasive pulmonary aspergillosis in immunocompromised patients. Infection starts with
the inhalation of A. fumigatus conidia that germinate in the lung. Professional phagocytes like alveolar macrophages contribute to the efficient clearance
of fungi from the lung by phagocytosis and degradation of conidia followed by release of chemokines and cytokines in order to trigger neutrophil
migration at the site of infection. In the immunocompromized host, at least some conidia are able to evade macrophage degradation, resulting in
germination and outgrowth of intracellularly residing spores. Therefore, conidia must be able to evade recognition and processing by phagocytes. The
avirulent pksP mutant of A. fumigatus lacking the melanin layer present on wild-type conidia exhibited increased phagocytosis by macrophages apparently
due to the loss of masking immunogenic glucan-structures. Furthermore, by analysing phagolysosome fusion and acidification we show that intracellular
processing of pksP mutant conidia is drastically increased in comparison to wild-type conidia, suggesting that A. fumigatus conidia interfere with the
endocytosis pathway, similar to obligate human pathogens like Legionella sp. or Mycobacterium sp.. The process by which wild-type conidia mediate
endocytotic alterations seems to be connected to the surface structure of melanized conidia but is independent of the presence of a functional
RodA-derived rodlet layer. Moreover, inhibition of phagolysosome acidification by macrophages is controlled by the fungal cAMP signaling pathway.

Abstract Number: NULL

Conference Year: 2011

Link to conference website: NULL

New link: NULL

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