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bioRxiv · 10.64898/2026.10.26.760590

Human Gut Microbiota of Healthy Individuals Show Resilience to Acute Aflatoxin B1 Exposure Despite Solvent-Driven Community Shifts

Abstract

Aflatoxin B1 (AFB1) is a potent mycotoxin linked to severe systemic health issues and gut microbiome disruption in in vivo models. However, it remains unclear whether AFB1 directly impairs human gut microbial composition and function or if observed dysbiosis is host-mediated. The objective of this work was to investigate the direct impact of acute AFB1 exposure on human gut microbiota from healthy individuals using anaerobic batch bioreactors. Fecal inoculum from 17 healthy adults was exposed to AFB1 concentrations ranging from 1,000 to 5,000 ppb, delivered in two solvents (ethanol and corn oil) under conditions simulating the large intestine. Metabolic activity was assessed via short-chain fatty acid (SCFA) and gas production measurements, while community structure was assessed using 16S rRNA gene amplicon sequencing. AFB1 concentrations remained stable throughout the incubations, indicating no significant microbial degradation of AFB1. Results showed that AFB1 did not significantly alter microbial SCFA output or community composition compared to solvent-only controls. Observed shifts in microbial profiles were primarily driven by the solvents used to bring AFB1 into solution rather than by the toxin. These findings demonstrate that healthy human gut microbial communities are resilient to direct, acute AFB1 exposure even at concentrations exceeding typical dietary levels. This suggests that microbiome disruption reported in vivo may be an indirect consequence of host-mediated factors, such as reactive metabolites or systemic immune responses, rather than direct toxicity by the parent compound.

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BibTeXRIS

Glesener, H., Dorn, N., Cheng, Q., Voth-Gaeddert, L., Krajmalnik-Brown, R.. 2026-10-27. Human Gut Microbiota of Healthy Individuals Show Resilience to Acute Aflatoxin B1 Exposure Despite Solvent-Driven Community Shifts. https://doi.org/10.64898/2026.10.26.760590

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