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PreprintCC BYbioRxiv

Oleic acid suppresses NLRP3 inflammasome activation to prevent dermal macrophage death and limit imiquimod-induced psoriasis

  • B. Burger
  • R. N. Sagiorato
  • I. B. Baccarin
  • V. R. Munoz
  • G. Cerna
  • I. Andreev
  • N. Araujo
  • H. S. Shu
  • J. Zhao
  • B. Sullivan
  • Y. Liang
  • R. A. M. Bistaffa
11 more authors
  • V. C. Gaspar
  • E. M. Yabuuti
  • N. B. Ramos
  • L. P. Pral
  • C. Evavold
  • J. C. A. Filho
  • P. Varga-Weisz
  • C. H. C. Serezani
  • M. A. R. Vinolo
  • H. M. Silva
  • H. G. Rodrigues1
  1. 1University of Campinas
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Abstract

Psoriasis is associated with altered lipid metabolism, including reduced expression of fatty acid metabolism genes and decreased circulating oleic acid. Here we report that oral oleic acid supplementation normalized serum oleic acid levels and protected from skin thickening and epidermal hyperplasia in a imiquimod mice model of psoriasis. These effects were associated with preserved skin-resident macrophage numbers and reduced expression of key psoriasis-associated inflammatory markers. Mechanistically, imiquimod induces dermal macrophage death via NLRP3/caspase-1 inflammasome activation, while adoptive transfer of dermal macrophages attenuates psoriasiform inflammation. Oleic acid rescued macrophages from imiquimod and nigericin-induced death in vitro by suppressing NF-{kappa}B and NLRP3/caspase-1 signaling, lowering IL-1{beta} and reactive oxygen species production, and restoring mitochondrial homeostasis, independently of TLR7. Together, our results position dermal macrophage survival as a previously unrecognized checkpoint in psoriasiform inflammation, and suggest that restoring lipid metabolic fitness, rather than solely targeting downstream inflammatory mediators, may offer an additional mechanism-based strategy to limit tissue- damaging inflammation.

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Cite

BibTeXRIS
BibTeX
@misc{burger2026oleic,
  title = {{Oleic acid suppresses NLRP3 inflammasome activation to prevent dermal macrophage death and limit imiquimod-induced psoriasis}},
  author = {B. Burger and R. N. Sagiorato and I. B. Baccarin and V. R. Munoz and G. Cerna and I. Andreev and N. Araujo and H. S. Shu and J. Zhao and B. Sullivan and Y. Liang and R. A. M. Bistaffa and V. C. Gaspar and E. M. Yabuuti and N. B. Ramos and L. P. Pral and C. Evavold and J. C. A. Filho and P. Varga-Weisz and C. H. C. Serezani and M. A. R. Vinolo and H. M. Silva and H. G. Rodrigues},
  howpublished = {bioRxiv},
  year = {2026},
  month = oct,
  doi = {10.64898/2026.10.27.760067},
  url = {https://www.biorxiv.org/content/10.64898/2026.10.27.760067v1},
  note = {CC BY},
}
RIS
TY  - UNPB
TI  - Oleic acid suppresses NLRP3 inflammasome activation to prevent dermal macrophage death and limit imiquimod-induced psoriasis
AU  - B. Burger
AU  - R. N. Sagiorato
AU  - I. B. Baccarin
AU  - V. R. Munoz
AU  - G. Cerna
AU  - I. Andreev
AU  - N. Araujo
AU  - H. S. Shu
AU  - J. Zhao
AU  - B. Sullivan
AU  - Y. Liang
AU  - R. A. M. Bistaffa
AU  - V. C. Gaspar
AU  - E. M. Yabuuti
AU  - N. B. Ramos
AU  - L. P. Pral
AU  - C. Evavold
AU  - J. C. A. Filho
AU  - P. Varga-Weisz
AU  - C. H. C. Serezani
AU  - M. A. R. Vinolo
AU  - H. M. Silva
AU  - H. G. Rodrigues
PY  - 2026
DA  - 2026/10/27
PB  - bioRxiv
DO  - 10.64898/2026.10.27.760067
UR  - https://www.biorxiv.org/content/10.64898/2026.10.27.760067v1
AB  - Psoriasis is associated with altered lipid metabolism, including reduced expression of fatty acid metabolism genes and decreased circulating oleic acid. Here we report that oral oleic acid supplementation normalized serum oleic acid levels and protected from skin thickening and epidermal hyperplasia in a imiquimod mice model of psoriasis. These effects were associated with preserved skin-resident macrophage numbers and reduced expression of key psoriasis-associated inflammatory markers. Mechanistically, imiquimod induces dermal macrophage death via NLRP3/caspase-1 inflammasome activation, while adoptive transfer of dermal macrophages attenuates psoriasiform inflammation. Oleic acid rescued macrophages from imiquimod and nigericin-induced death in vitro by suppressing NF-{kappa}B and NLRP3/caspase-1 signaling, lowering IL-1{beta} and reactive oxygen species production, and restoring mitochondrial homeostasis, independently of TLR7. Together, our results position dermal macrophage survival as a previously unrecognized checkpoint in psoriasiform inflammation, and suggest that restoring lipid metabolic fitness, rather than solely targeting downstream inflammatory mediators, may offer an additional mechanism-based strategy to limit tissue- damaging inflammation.
ER  -