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Resolution of inflammation: the beginning programs the end
Abstract
Acute inflammation normally resolves by mechanisms that have remained somewhat elusive. Emerging evidence now suggests that an active, coordinated program of resolution initiates in the first few hours after an inflammatory response begins. After entering tissues, granulocytes promote the switch of arachidonic acid-derived prostaglandins and leukotrienes to lipoxins, which initiate the termination sequence. Neutrophil recruitment thus ceases and programmed death by apoptosis is engaged. These events coincide with the biosynthesis, from omega-3 polyunsaturated fatty acids, of resolvins and protectins, which critically shorten the period of neutrophil infiltration by initiating apoptosis. Consequently, apoptotic neutrophils undergo phagocytosis by macrophages, leading to neutrophil clearance and release of anti-inflammatory and reparative cytokines such as transforming growth factor-beta1. The anti-inflammatory program ends with the departure of macrophages through the lymphatics. Understanding these and further details of the mechanism required for inflammation resolution may underpin the development of drugs that can resolve inflammatory processes in directed and controlled ways.
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“In conclusion, attenuating inflammation itself might also interfere with successful resolution, since the process of resolution is initiated already very early during the inflammatory process.441”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [441]
In the citing paper
“Conceptually, results of our study support the idea that excessive fibrotic response is a direct result of a “failed” resolution of sterile inflammation35, with impaired phagocytosis of injured hepatocytes enabling exposure of quiescent stellate cells to fibrogenic mito-DAMPs.”
From Hepatocyte mitochondria-derived danger signals directly activate hepatic stellate cells and drive progression of liver fibrosis (2020) · cites this paper as [35]
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“Thus, PPAR␥ is important to shape an anti-inflammatory macrophage phenotype and appears crucial for dampening inflammation (15).”
From MicroRNA-27b Contributes to Lipopolysaccharide-mediated Peroxisome Proliferator-activated Receptor γ (PPARγ) mRNA Destabilization (2010) · cites this paper as [15]
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Metadata
- Authors
- Serhan, C. N., & Savill, J.
- Affiliations
- Brigham and Women's Hospital (US)
- Centre for Inflammation Research (GB)
- Corresponding author
- Serhan, Charles N
- Venue
- Nature Immunology
- Published
- 2005-11-17
- Volume
- 6
- Issue
- 12
- Pages
- 1191-1197
- ISSN
- 1529-2908 (ISSN-L)
- 1529-2916
- OpenAlex
- W2004536682
- Cited by
- 2,552
- References
- 80
- Citations by year
- 2026: 107 · 2025: 94 · 2024: 105 · 2023: 119 · 2022: 141 · 2021: 153 · 2020: 131 · 2019: 123 · 2018: 117 · 2017: 137 · 2016: 100 · 2015: 128 · 2014: 161 · 2013: 157 · 2012: 139
- FWCI
- 11.93
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Wellcome Trust
- National Institute of General Medical Sciences (GM 38765)
- National Institute of Dental and Craniofacial Research (P50DE016191)
- Topics
- Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Health Sciences › Medicine › Pharmacology (medical) › Inflammatory mediators and NSAID effects
- Keywords
- inflammation resolution, acute inflammation, lipoxins, resolvins, protectins, omega-3 polyunsaturated fatty acids, arachidonic acid metabolites, prostaglandins, leukotrienes, neutrophil apoptosis, neutrophil clearance, macrophage phagocytosis, TGF-β1, anti-inflammatory cytokines, anti-inflammatory drug development
- MeSH terms
- Acute Disease, Animals, Humans, Inflammation
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