{"hq_id":"hq-c-org-002094","name":"Gliotoxin","context":"human_adult","risk_level":"moderate","schema":"legacy","note":"Synthesis unavailable: compound lacks vectorizable regulatory classifications. Raw safety data returned.","data":{"risk_level":"moderate","summary":"Gliotoxin is an epipolythiodioxopiperazine (ETP) mycotoxin produced primarily by Aspergillus fumigatus, the leading cause of invasive aspergillosis. It is a key virulence factor that enables A. fumigatus to evade host immune defenses. Mechanism: the disulfide bridge in gliotoxin inhibits NF-kB activation by preventing IkB-alpha degradation, thereby suppressing pro-inflammatory cytokine production. It also induces apoptosis in immune cells (neutrophils, monocytes, dendritic cells) via mitochondrial membrane depolarization and caspase activation. Gliotoxin is detectable in serum and bronchoalveolar lavage fluid of patients with invasive aspergillosis, and serum levels correlate with disease severity and prognosis. It is genotoxic (DNA strand breaks) and immunosuppressive at sub-cytotoxic concentrations. Clinical significance: gliotoxin contributes to the 30-90% mortality rate of invasive aspergillosis in immunocompromised patients. It has been explored as a potential biomarker for invasive aspergillosis. Not regulated as a food contaminant. Primary concern is as a virulence factor in clinical mycology.","source_refs":["aletheia_fungi_batch_2026"]},"meta":{"synthesis_version":"n/a","timestamp":"2026-05-14T01:22:10.782Z"}}