Angiogenesis at the mold-host interface: A potential key to understanding and treating invasive aspergillosis

Ronen Ben-Ami

Research output: Contribution to journalReview articlepeer-review

Abstract

Invasive aspergillosis (IA) in neutropenic patients is characterized by angioinvasion, intravascular thrombosis and tissue infarction, features that lead to sequestration of infected tissue and impaired fungal clearance. Recent research has shown that host angiogenesis, the homeostatic compensatory response to tissue hypoxia, is downregulated by Aspergillus fumigatus secondary metabolites. A. fumigatus metabolites inhibit multiple key angiogenic mediators, notably basic FGF, VEGF and their respective receptors. Moreover, repletion of basic FGF and VEGF enhances angiogenesis at the site of infection, induces trafficking of polymorphonuclear leukocytes into fungal-infected tissue and enhances antifungal drug activity. This review summarizes the emerging roles of vasculopathy and angiogenesis in the pathogenesis of IA, emphasizing the importance of the underlying mode of immunosuppression. Modulation of angiogenesis is a potential target for novel therapeutic strategies against IA.

Original languageEnglish
Pages (from-to)1453-1462
Number of pages10
JournalFuture Microbiology
Volume8
Issue number11
DOIs
StatePublished - Nov 2013

Keywords

  • angiogenesis
  • FGF
  • gliotoxin
  • invasive aspergillosis
  • secondary metabolism
  • VEGF

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