Human macrophages differentially produce specific resolvin or leukotriene signals that depend on bacterial pathogenicity

Oliver Werz (), Jana Gerstmeier, Stephania Libreros, Xavier De la Rosa, Markus Werner, Paul C. Norris, Nan Chiang and Charles N. Serhan ()
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Oliver Werz: Brigham and Women’s Hospital and Harvard Medical School
Jana Gerstmeier: Friedrich-Schiller-University Jena
Stephania Libreros: Brigham and Women’s Hospital and Harvard Medical School
Xavier De la Rosa: Brigham and Women’s Hospital and Harvard Medical School
Markus Werner: Friedrich-Schiller-University Jena
Paul C. Norris: Brigham and Women’s Hospital and Harvard Medical School
Nan Chiang: Brigham and Women’s Hospital and Harvard Medical School
Charles N. Serhan: Brigham and Women’s Hospital and Harvard Medical School

Nature Communications, 2018, vol. 9, issue 1, 1-12

Abstract: Abstract Proinflammatory eicosanoids (prostaglandins and leukotrienes) and specialized pro-resolving mediators (SPM) are temporally regulated during infections. Here we show that human macrophage phenotypes biosynthesize unique lipid mediator signatures when exposed to pathogenic bacteria. E. coli and S. aureus each stimulate predominantly proinflammatory 5-lipoxygenase (LOX) and cyclooxygenase pathways (i.e., leukotriene B4 and prostaglandin E2) in M1 macrophages. These pathogens stimulate M2 macrophages to produce SPMs including resolvin D2 (RvD2), RvD5, and maresin-1. E. coli activates M2 macrophages to translocate 5-LOX and 15-LOX-1 to different subcellular locales in a Ca2+-dependent manner. Neither attenuated nor non-pathogenic E. coli mobilize Ca2+ or activate LOXs, rather these bacteria stimulate prostaglandin production. RvD5 is more potent than leukotriene B4 at enhancing macrophage phagocytosis. These results indicate that M1 and M2 macrophages respond to pathogenic bacteria differently, producing either leukotrienes or resolvins that further distinguish inflammatory or pro-resolving phenotypes.

Date: 2018
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DOI: 10.1038/s41467-017-02538-5

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