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Galectin-1 induces 12/15-lipoxygenase expression in murine macrophages and favors their conversion toward a
Ran Rostoker1, Hiba Yaseen, Sagie Schif-Zuck
1Department of Biology, Faculty of Natural Sciences, University of Haifa, Haifa 31905, Israel.
Abstract:
During the resolution of inflammation macrophages undergo functional changes upon exposure to pro-resolving agents in their microenvironment. Primarily, engulfment of apoptotic polymorphonuclear (PMN) cells promotes conversion of macrophages toward a pro-resolving phenotype characterized by reduced CD11b expression. These macrophages are not phagocytic, do not respond to TLR ligands, and express relatively high levels of the pro-resolving enzyme 12/15-lipoxygenase (LO). Here, we report that the immuno-regulatory lectin galectin-1 is selectively expressed by CD11b(high), but not CD11b(low) macrophages. Upon exposure in vivo and ex vivo, galectin-1 directly promoted macrophage conversion from a CD11b(high) to a CD11b(low) phenotype and up-regulated the expression and activity of 12/15-LO. Moreover, galectin-1 treatment in vivo promoted the loss of phagocytic capacity (efferocytic satiation) in peritoneal macrophages and down-regulated secretion of TNF-α, IL-1β, and IL-10 upon LPS exposure. Our results suggest that galectin-1 could be an essential mediator in the control of macrophage function during the resolution of inflammation.
Insights
Galectin-1 drives macrophage conversion to a pro-resolving phenotype by reducing CD11b expression and enhancing 12/15-lipoxygenase (LO) activity, aiding inflammation resolution.
Area of Science:
- Immunology
- Cell Biology
- Inflammation Resolution
Background:
- Macrophages shift phenotype during inflammation resolution.
- Engulfment of apoptotic polymorphonuclear (PMN) cells induces a pro-resolving macrophage phenotype with reduced CD11b expression and increased 12/15-lipoxygenase (LO).
Purpose of the Study:
- To investigate the role of galectin-1 in regulating macrophage phenotype during inflammation resolution.
- To determine if galectin-1 mediates the conversion of macrophages to a pro-resolving state.
Main Methods:
- In vivo and ex vivo experiments using galectin-1.
- Analysis of CD11b expression, 12/15-LO expression and activity, phagocytic capacity, and cytokine secretion (TNF-α, IL-1β, IL-10) in macrophages.
- Lipopolysaccharide (LPS) challenge was used to assess macrophage response.
Main Results:
- Galectin-1 is selectively expressed by CD11b(high) macrophages.
- Galectin-1 treatment induced a shift from CD11b(high) to CD11b(low) macrophage phenotype.
- Galectin-1 up-regulated 12/15-LO expression and activity, reduced phagocytic capacity (efferocytic satiation), and down-regulated pro-inflammatory cytokine secretion upon LPS exposure.
Conclusions:
- Galectin-1 is a key regulator of macrophage functional changes during inflammation resolution.
- Galectin-1 promotes a pro-resolving macrophage phenotype, characterized by reduced CD11b and enhanced 12/15-LO.
- Galectin-1 plays a critical role in controlling macrophage behavior for effective resolution of inflammation.
