A noncanonical polyamine from bacteria antagonizes host mitochondrial function.

ABSTRACT: Interactions between gut bacterial polyamines and intestinal cells have been proposed to contribute to inflammatory bowel diseases, but the underlying molecular mechanisms are often unclear. Here, we use a derivatization-based LC-MS approach and the model animal Caenorhabditis elegans to study microbiome-derived polyamine bioactivity. We show that aberrant polyamine metabolism in two diverse bacterial species (Escherichia coli K12 and Bacillus subtilis 168) can result in the accumulation of a noncanonical polyamine intermediate, N¹-aminopropylagmatine (N¹-APA). N¹-APA is produced via spermidine synthase (SpeE) and is bioactive in C. elegans intestinal cells and mouse bone marrow macrophages. Specifically, bacterial N¹-APA can be transported into

SUBMITTER: Nauta KM 

PROVIDER: S-EPMC12749970 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature