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DDS promotes longevity through a microbiome-mediated starvation signal.

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The antibiotic diaminodiphenyl sulfone (DDS) extends lifespan in C. elegans by reducing microbiome folate production. This novel mechanism, distinct from its known effects, relies on FMO-2 and mimics metformin

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Area of Science:

  • Microbiology and Aging Research
  • Microbiome-Host Interactions
  • Drug Mechanisms of Action

Background:

  • Leprosy is treated with diaminodiphenyl sulfone (DDS) alongside other antibiotics.
  • DDS is known to extend lifespan in *C. elegans* by inhibiting pyruvate kinase and reducing mitochondrial function.
  • The microbiome's role in drug efficacy and host longevity is an emerging area of research.

Purpose of the Study:

  • To investigate an alternative mechanism by which DDS promotes longevity in *C. elegans*.
  • To explore the role of the microbiome in DDS-mediated lifespan extension.
  • To identify specific molecular pathways involved in this novel DDS mechanism.

Main Methods:

  • Utilized *C. elegans* as a model organism.
  • Investigated the impact of DDS on microbiome folate production.
  • Analyzed changes in methionine cycle metabolites.
  • Assessed the dependence of lifespan extension on FMO-2, a flavin-containing monooxygenase.

Main Results:

  • DDS was found to reduce folate production by the *C. elegans* microbiome.
  • This reduction led to altered methionine cycle metabolite levels, similar to metformin's effects.
  • Lifespan extension by DDS was dependent on FMO-2, particularly under starvation and hypoxia conditions.

Conclusions:

  • DDS promotes longevity in *C. elegans* through a novel mechanism involving reduced microbiome folate production.
  • This pathway is independent of DDS's previously known effects on pyruvate kinase and mitochondria.
  • The findings highlight the importance of microbiome-host interactions in drug-induced longevity and identify FMO-2 as a key mediator.