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2016 ; 4
(3
): ä Nephropedia Template TP
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Macrophage Proresolving Mediators-the When and Where
#MMPMID27337457
Dalli J
; Serhan C
Microbiol Spectr
2016[Jun]; 4
(3
): ä PMID27337457
show ga
Macrophages and neutrophils orchestrate acute inflammation and host defense as
well as the resolution phase and return to homeostasis. In this article, we
review the contribution of macrophages to local lipid mediator (LM) levels and
the regulation of macrophage LM profiles by polymorphonuclear neutrophils and
neutrophil-derived microparticles. We carried out LM metabololipidomics,
profiling distinct phagocytes: neutrophils (PMNs), apoptotic PMNs, and
macrophages. Efferocytosis increased specialized proresolving mediator (SPM)
biosynthesis, including resolvin D1 (RvD1), RvD2, and RvE2, which were further
elevated by PMN microparticles. In studies using deuterium-labeled precursors
(d8-arachidonic acid, d5-eicosapentaenoic acid, and d5-docosahexaenoic acid),
apoptotic PMNs and microparticles contributed to SPM biosynthesis during
efferocytosis. Assessment of macrophage LM profiles in M2 macrophages
demonstrated higher SPM levels in this macrophage subset, including maresin 1
(MaR1), and lower amounts of leukotriene B4 (LTB4) and prostaglandins than in M1.
Apoptotic PMN uptake by both macrophage subtypes led to modulation of their LM
profiles. LTB4 was downregulated in M2, whereas SPMs including lipoxin A4 were
increased. Conversely, uptake of apoptotic PMNs by M2 macrophages reduced (?25%)
overall LMs. MaR1 displays potent tissue-regenerative and antinociceptive actions
in addition to its proresolving and anti-inflammatory actions. In addition, the
MaR1 biosynthetic intermediate 13S,14S-epoxy-maresin is also bioactive,
inhibiting LTB4 biosynthesis and switching macrophage phenotypes from M1 to M2.
Together, these results establish LM signature profiles of human phagocytes and
related subpopulations. They demonstrate microparticle regulation of
macrophage-specific endogenous LMs during defined stages of acute inflammation
and their dynamic changes in human primary phagocytes.
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