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<p>Parkinson’s disease (PD) is a no-curable neurodegenerative disease of pandemic distribution for which only palliative treatments are available. A hallmark of PD is injury to dopaminergic neurons in the substantia nigra pars compacta. Here, we report that <i>Caenorhabditis elegans</i> colonized by biofilm-forming <i>Bacillus subtilis</i> is resistant to injury of dopaminergic neurons caused by treatment with the PD-related neurotoxin 6-hydroxydopamine (6-OHDA). Biofilm-forming <i>B. subtilis</i>-colonized <i>C. elegans</i> display dopamine-dependent behaviors indistinguishable from those of 6-OHDA-untreated worms colonized by gut commensal <i>E. coli</i> OP50. In <i>C. elegans</i> PD model strains with early dopaminergic neuron decay or overexpressing human alpha-synuclein, biofilm-forming <i>B. subtilis</i> colonization had neuroprotective effects and prevents alpha-synulcein aggregation, respectively. The <i>B. subtilis</i>-controlled insulin/IGF-1 signaling (ILS), whose downregulation prevents aging-related PD, is not involved in protecting against 6-OHDA-related injury. We demonstrate that biofilm-forming <i>B. subtilis</i> activates PMK-1 (p38 MAPK)/SKN-1 (Nrf2) signaling, which protects <i>C. elegans</i> from 6-OHDA-induced dopaminergic neuron injury.</p>

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Biofilm proficient Bacillus subtilis prevents neurodegeneration in Caenorhabditis elegans Parkinson’s disease models via PMK-1/p38 MAPK and SKN-1/Nrf2 signaling

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年3月21日

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  • Marcos Francisco,
  • Roberto Grau

摘要

Parkinson’s disease (PD) is a no-curable neurodegenerative disease of pandemic distribution for which only palliative treatments are available. A hallmark of PD is injury to dopaminergic neurons in the substantia nigra pars compacta. Here, we report that Caenorhabditis elegans colonized by biofilm-forming Bacillus subtilis is resistant to injury of dopaminergic neurons caused by treatment with the PD-related neurotoxin 6-hydroxydopamine (6-OHDA). Biofilm-forming B. subtilis-colonized C. elegans display dopamine-dependent behaviors indistinguishable from those of 6-OHDA-untreated worms colonized by gut commensal E. coli OP50. In C. elegans PD model strains with early dopaminergic neuron decay or overexpressing human alpha-synuclein, biofilm-forming B. subtilis colonization had neuroprotective effects and prevents alpha-synulcein aggregation, respectively. The B. subtilis-controlled insulin/IGF-1 signaling (ILS), whose downregulation prevents aging-related PD, is not involved in protecting against 6-OHDA-related injury. We demonstrate that biofilm-forming B. subtilis activates PMK-1 (p38 MAPK)/SKN-1 (Nrf2) signaling, which protects C. elegans from 6-OHDA-induced dopaminergic neuron injury.