Biology subjects

Voth-Gaeddert, L.

Publications and source records attributed to Voth-Gaeddert, L..

2 recordsLinked to original sources

bioRxiv2026

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

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.

microbiology↗

bioRxiv2026

Cholera toxin remodels intestinal immunity and suppresses systemic metabolism

Cholera toxin (CTx) is a potent enterotoxin and widely used mucosal adjuvant, yet the acute host response to CTx itself, in the absence of a co-administered antigen, remains vague. In this study, we integrated physiological and metabolic phenotyping with intestinal transcriptomics, epithelial imaging, immune profiling, hepatic gene-expression analysis, and paired microbiome profiling to characterize the response to a single oral CTx exposure in mice. Within 24 h, CTx remodeled immune-cell composition in both epithelial and lamina propria compartments, with responses shaped by sex and genetic background. Recurrent changes included increased epithelial group 3 innate lymphoid cells, reduced lamina propria ROR{gamma}t+ regulatory T cells, and decreased epithelial ILC1/NK cells in males of both strains. CTx also increased villus DCLK1+ tuft cells and reduced MUC2 immunoreactivity. Jejunal transcriptomics revealed induction of inflammatory defense, glycolytic, autophagy, and lipid-utilization programs together with suppression of proliferative and mitochondrial programs, consistent with coordinated stress adaptation. These local changes were accompanied by rapid restructuring of the fecal microbial community and by systemic hypometabolism, despite markedly different hypothermic responses across strains. CTx also elicited a selective hepatic stress and metabolic program, including conserved suppression of Cyp7a1 across sexes and strains. Together, these findings show that CTx alone rapidly reorganizes the intestinal immune, epithelial, metabolic, and microbial environment while suppressing whole-body metabolism. This work provides an integrated framework for understanding the acute host response to CTx and for interpreting its widespread use as a mucosal adjuvant.

immunology↗