{
  "abstract": "Pathogen infection profoundly remodels host metabolism. Whether hosts sense specific pathogen-induced metabolic changes to identify microbial infection is not known. Here, we find that depletion the monounsaturated fatty acid oleate is a metabolic pattern of pathogenesis, specifically surveilled by the nematode C. elegans to identify active infection with a bacterial pathogen. We previously demonstrated that the enzymatic TIR (Toll/interleukin-1 receptor/resistance)-domain containing protein, TIR-1/SARM1, the key upstream activator of p38 MAPK PMK-1 immunity, is a guard protein in an effector-triggered immune response, positioned specifically on the surface of lysosome-related organelles to sense the toxic effects of bacterial infection. Here, we show that acute loss of oleate in intestinal cells during bacterial infection causes lysosome-related organelles to collapse, which induces the aggregation and activation of TIR-1/SARM1. Further, we find that oleate deficiency is a host vulnerability that concomitantly activates the c-Jun N-terminal kinase (JNK) KGB-1 nutrient sensing pathway, an adaptive response that promotes expression of TIR-1/SARM1 on lysosome-related organelles and is required for survival during infection. These data establish a mechanistic connection between fatty acid nutrition and innate immune regulation, and reveal that specific changes in host metabolism are surveilled to identify pathogen attack.",
  "abstract_shown": true,
  "affiliations": [
    "University of Massachusetts Medical School"
  ],
  "article_type": "New results",
  "arxiv": null,
  "author_total": 3,
  "authors": [
    {
      "name": "K. A. Wani"
    },
    {
      "name": "S. S. Rahman"
    },
    {
      "affs": [
        0
      ],
      "name": "R. Pukkila-Worley"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/0tdsarqrz7ker.bib",
  "cited_by": 0,
  "doi": "10.64898/2026.11.04.764347",
  "fulltext_url": "https://www.biorxiv.org/content/10.64898/2026.11.04.764347v1.full",
  "id": "0tdsarqrz7ker",
  "issns": [],
  "landing_url": "https://www.biorxiv.org/content/10.64898/2026.11.04.764347v1",
  "language": null,
  "licence": "CC-BY",
  "licence_label": "CC BY",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "biorxiv",
      "immunology"
    ]
  ],
  "openalex": null,
  "pdf_url": "https://www.biorxiv.org/content/10.64898/2026.11.04.764347v1.full.pdf",
  "pmcid": null,
  "pmid": null,
  "published": "2026-11-04",
  "publisher": null,
  "ris": "https://research.draconitic.com/paper/0tdsarqrz7ker.ris",
  "sources": [
    {
      "first_seen": "2026-11-06T12:21:04Z",
      "native_id": "10.64898/2026.11.04.764347",
      "source": "biorxiv",
      "url": "https://www.biorxiv.org/content/10.64898/2026.11.04.764347v1"
    }
  ],
  "subjects": [
    {
      "field": "biology",
      "origin": "biorxiv:immunology",
      "subfield": "immunology"
    }
  ],
  "title": "Monounsaturated fatty acid depletion is a metabolic pattern of pathogenesis surveilled to activate p38 MAPK innate immunity",
  "title_text": "Monounsaturated fatty acid depletion is a metabolic pattern of pathogenesis surveilled to activate p38 MAPK innate immunity",
  "type": "preprint",
  "updated_at": "2026-11-08T00:21:02Z",
  "url": "https://research.draconitic.com/paper/0tdsarqrz7ker",
  "venue": "bioRxiv",
  "versions": []
}