<p>The gut microbiota is increasingly recognized as a key contributor to intestinal and brain pathologies, including Parkinson’s disease (PD). Sulfate-reducing <i>Desulfovibrio</i> (DSV) species have emerged as microbial drivers through hydrogen sulfide and other neurotoxic factors. Using the <i>Caenorhabditis elegans</i> PD model NL5901 expressing human α-synuclein, we examined the effects of six DSV strains from human, animal, and environmental sources on food preference, α-syn aggregation, ROS production, gene expression, and lifespan. <i>C. elegans</i> strongly preferred environmental strains, particularly <i>D. vulgaris</i> DSM 644 (94.7% vs. 5.3% over <i>D. piger</i> DSM 749). In contrast, the animal isolate <i>D. desulfuricans</i> DSM 6949 and PD isolate <i>D</i>. spp. MUU 26 induced the highest α-syn aggregation (49.05 and 40.15 aggregates), ROS (3.42-fold, 3.01-fold), and <i>sod-3</i>, <i>daf-16</i>, and <i>hsp-16.1</i> repression. DSM 644-fed worms exhibited a protective transcriptional profile and the greatest lifespan extension (median 36 days). These results highlight strain-specific effects of DSV on neurodegeneration, oxidative stress, and aging, reinforcing the need for mechanistic validation in mammalian PD models.</p>

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Strain-specific effects of Desulfovibrio on neurodegeneration and oxidative stress in a Caenorhabditis elegans PD model

  • Khosrow Mohammadi,
  • Dongming Zhang,
  • Per Erik Joakim Saris

摘要

The gut microbiota is increasingly recognized as a key contributor to intestinal and brain pathologies, including Parkinson’s disease (PD). Sulfate-reducing Desulfovibrio (DSV) species have emerged as microbial drivers through hydrogen sulfide and other neurotoxic factors. Using the Caenorhabditis elegans PD model NL5901 expressing human α-synuclein, we examined the effects of six DSV strains from human, animal, and environmental sources on food preference, α-syn aggregation, ROS production, gene expression, and lifespan. C. elegans strongly preferred environmental strains, particularly D. vulgaris DSM 644 (94.7% vs. 5.3% over D. piger DSM 749). In contrast, the animal isolate D. desulfuricans DSM 6949 and PD isolate D. spp. MUU 26 induced the highest α-syn aggregation (49.05 and 40.15 aggregates), ROS (3.42-fold, 3.01-fold), and sod-3, daf-16, and hsp-16.1 repression. DSM 644-fed worms exhibited a protective transcriptional profile and the greatest lifespan extension (median 36 days). These results highlight strain-specific effects of DSV on neurodegeneration, oxidative stress, and aging, reinforcing the need for mechanistic validation in mammalian PD models.