ArticleCell death & disease2026
Alox8 knockout exacerbates imiquimod-induced psoriasis-like inflammation.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Lipoxygenases peroxidise polyunsaturated fatty acids, resulting in oxylipins, which may act pro- or anti-inflammatory. Arachidonate 15-lipoxygenase type B was shown to play a role in the resolution of keratinocyte inflammation and is upregulated in psoriasis. Its murine ortholog, arachidonate 8-lipoxygenase (Alox8), differs in regiospecificity in that it adds molecular oxygen to the 8th and not 15th carbon of arachidonic acid. This study aimed to determine if Alox8 plays a role in the resolution of murine imiquimod-induced psoriasis. Alox8 knockout (KO) mice, which are not commercially available, were generated with a functional KO targeting the enzyme's active site. Untargeted Lipidomics revealed changes in the skin lipidome from both imiquimod-induced psoriasis as well as between wild-type and KO mice. Furthermore, LC-MS/MS revealed a functional KO with reductions in Alox8-specific oxylipins. Lipid peroxidation marker 4-hydroxynonenal was elevated in the epidermis of wild-type mice from imiquimod treatment, however, it was significantly reduced in Alox8 KO mice. Alox8 KO mice exhibited a thickened epidermis, resulting from reduced DNA damage and increased proliferation. Moreover, immune cell infiltration was enhanced in Alox8 KO mice, including a higher abundance of γδ T cells. Elevated cytokine levels of interleukin-17 and -22, accompanied by keratinocyte-produced C-X-C motif chemokine ligand 1, were detected in the skin of Alox8 KO mice. Additionally, cyclooxygenase 2 expression and prostaglandin E
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