Aspergillus fumigatus infection is responsible for approximately 4% of all hospital-based deaths in Europe. The organism is an opportunistic fungal pathogen of immunocompromised patients and is the commonest etiological agent of invasive aspergillosis (IA). Gliotoxin is produced by A. fumigatus and is primarily described in terms of its cytotoxicity towards animal cells. In our recent work [1] and preliminary data suggests that significant new thinking is necessary to understand the role of gliotoxin in A. fumigatus because, under certain conditions, it appears to induce major redox dysregulation in the organism. We were the first to demonstrate that gliT, a gliotoxin oxidoreductase gene in the gliotoxin (gli) biosynthetic cluster, is essential to protect A. fumigatus against the deleterious effects of exogenously- added gliotoxin. However, the precise mechanism of gliotoxin self-protection, and trans effects of gliotoxin presence, remain obscure.
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