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Ovezgeldiyev, D.* ; Trefzer, V.* ; Doolan, R.* ; Moyat, M.* ; Coakley, G.* ; Wickramasinghe, L.C.* ; Daunt, C.* ; Volpe, B.* ; Henkel, F. ; Serra, A.* ; Hartmann, M.* ; Rezaei, S.* ; Ubags, N.* ; Butler, A.* ; Chatzis, R.* ; Marsland, B.J.* ; Smith, A.A.T.* ; Deveson Lucas, D.* ; McGowan, E.N.S.* ; Binger, K.J.* ; McConville, M.J.* ; Esser-von Bieren, J. ; Harris, N.L.* ; Bouchery, T.*

Alox15 restrains glycolysis to support M2 macrophage effector function during helminth immunity.

J. Exp. Med. 223:e20241620 (2026)
DOI
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Macrophage polarization by type-2 cytokines is central to anti-helminth immunity and tissue repair. While some hallmark changes in macrophages are well-characterized and associated with protection against helminths, it is still unclear how macrophages exert their anti-helminth effects. In this context, we investigated arachidonate 15-lipoxygenase (LOX) (Alox15), a LOX well known for its role in macrophage polarization in the context of metabolic diseases, and a hallmark of type-2 macrophage (M2) human polarization. We show that in the absence of Alox15, M2 cannot trap and kill helminths. Surprisingly, expression of M2 markers was normal despite a loss of function. Instead, we found a concomitant increase in pro-inflammatory responses due to an uncontrolled activation of glycolysis. We further show that activation of Peroxisome proliferator-activated receptor-delta (PPAR-δ) by lipids downstream of docosapentaenoic acid (DPA) can restore normal glycolysis control, highlighting a novel role of lipids in the fine-tuning of the metabolic support required for optimal macrophage polarization.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Rna-seq; Gene-expression; 12/15-lipoxygenase; Responses; Repression; Resistance; Biology
ISSN (print) / ISBN 0022-1007
e-ISSN 1540-9538
Zeitschrift Journal of Experimental Medicine
Quellenangaben Band: 223, Heft: 10, Seiten: , Artikelnummer: e20241620 Supplement: ,
Verlag Rockefeller University Press
Verlagsort 950 Third Ave, 2nd Flr, New York, Ny 10022 Usa
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Allergy Research (IAF)
Förderungen Swiss National Science Foundation (SNF)
Swiss National Science Foundation
National Health and Medical Research Council
Monash Platform Access
German Research Foundation