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Area of Science:

  • Biochemistry
  • Immunology
  • Dermatology

Background:

  • Lipoxygenases produce oxylipins, influencing inflammation.
  • Arachidonate 15-lipoxygenase type B is implicated in keratinocyte inflammation resolution.
  • Murine arachidonate 8-lipoxygenase (Alox8) differs in oxygen addition site compared to human orthologs.

Purpose of the Study:

  • To investigate the role of Alox8 in resolving imiquimod-induced psoriasis in mice.
  • To characterize the effects of Alox8 deficiency on skin inflammation and lipid profiles.

Main Methods:

  • Generation of Alox8 knockout (KO) mice by targeting the enzyme's active site.
  • Untargeted lipidomics and LC-MS/MS analysis of skin samples.
  • Assessment of epidermal changes, immune cell infiltration, and cytokine/mediator levels.

Main Results:

  • Alox8 KO mice displayed exacerbated and prolonged psoriasis-like skin inflammation.
  • Reduced levels of Alox8-specific oxylipins and 4-hydroxynonenal were observed in Alox8 KO mice.
  • Alox8 deficiency led to increased epidermal thickness, immune cell infiltration (including γδ T cells), and elevated pro-inflammatory cytokines (IL-17, IL-22).

Conclusions:

  • Alox8 plays a significant role in the resolution of murine psoriasis.
  • Alox8 deficiency results in an exacerbated inflammatory phenotype, suggesting a protective role in skin inflammation.