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Lipid mediator class switching during acute inflammation: signals in resolution
B D Levy1, C B Clish, B Schmidt
1Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA.
Nature Immunology
|June 29, 2001
Summary
Leukotrienes and prostaglandins initiate inflammation, but lipoxins resolve it. This study shows how inflammatory mediators shift to anti-inflammatory ones, reprogramming immune cells to stop inflammation and promote healing.
Area of Science:
- Biochemistry
- Immunology
- Inflammation Research
Background:
- Leukotrienes (LTs) and prostaglandins (PGs) are key mediators that amplify acute inflammation.
- Lipoxins (LXs) possess distinct anti-inflammatory properties, counteracting inflammatory processes.
- Understanding the temporal dynamics of these lipid mediators is crucial for inflammation resolution.
Purpose of the Study:
- To investigate the temporal relationship between eicosanoids and immune cell recruitment in acute inflammation.
- To elucidate the mechanism by which inflammatory mediators shift towards anti-inflammatory lipid biosynthesis.
- To determine the role of specific eicosanoids in promoting the resolution of inflammation.
Main Methods:
- Temporal analysis of leukotrienes, prostaglandins, and lipoxins in clinical and experimental exudates.
- Investigating polymorphonuclear neutrophil (PMN) recruitment and behavior in inflammatory exudates.
- Examining eicosanoid biosynthesis switch in human peripheral blood PMNs exposed to prostaglandin E2 (PGE2).
Main Results:
- Early co-appearance of LTs and PGs correlated with PMN recruitment.
- Lipoxin biosynthesis followed, coinciding with spontaneous resolution of inflammation.
- PGE2 exposure induced a switch in PMNs from LTB4/5-lipoxygenase pathways to LXA4/15-lipoxygenase pathways, inhibiting PMN infiltration.
Conclusions:
- First-phase eicosanoids (LTs and PGs) play a role in initiating a shift towards anti-inflammatory lipid production.
- Distinct lipid mediator profiles dynamically change during acute exudate formation.
- This lipid mediator reprogramming of exudate PMNs is essential for promoting inflammation resolution.
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