Neutrophil cannibalism – a back up when the macrophage clearance system is insufficient
Open accessAbstract
BACKGROUND: During a lipopolysaccharide-induced lung inflammation, a massive accumulation of neutrophils occurs, which is normally cleared by macrophage phagocytosis following neutrophil apoptosis. However, in cases of extensive apoptosis the normal clearance system may fail, resulting in extensive neutrophil secondary necrosis. The aim of this study was to explore the hypothesis that neutrophils, in areas of the lung with extensive cellular infiltration, contribute to clearance by phagocytosing apoptotic cells and/or cell debris derived from secondary necrosis. METHODS: Intranasal lipopolysaccharide administration was used to induce lung inflammation in mice. The animals were sacrificed at seven time points following administration, bronchoalveolar lavage was performed and tissue samples obtained. Electron microscopy and histochemistry was used to assess neutrophil phagocytosis. RESULTS: Electron microscopic studies revealed that phagocytosing neutrophils was common, at 24 h after LPS administration almost 50% of the total number of neutrophils contained phagosomes, and the engulfed material was mainly derived from other neutrophils. Histochemistry on bronchoalvolar lavage cells further showed phagocytosing neutrophils to be frequently occurring. CONCLUSION: Neutrophils are previously known to phagocytose invading pathogens and harmful particles. However, this study demonstrates that neutrophils are also able to engulf apoptotic neutrophils or cell debris resulting from secondary necrosis of neutrophils. Neutrophils may thereby contribute to clearance and resolution of inflammation, thus acting as a back up system in situations when the macrophage clearance system is insufficient and/or overwhelmed.
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PMNs are essential to take over the job of efferocytosis when massive cell death occurs.
“PMNs are essential to take over the job when massive cell death occurs (130).”
From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [130]
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- Authors
- Rydell-Törmänen, K., Uller, L., & Erjefält, J. S.
- Affiliations
- Lund University (SE)
- ORCID
- Uller, Lena
- Venue
- Respiratory Research
- Published
- 2006-12
- Volume
- 7
- Issue
- 1
- Pages
- 143-143
- ISSN
- 1465-9921 (ISSN-L)
- 1465-993X
- PMC
- PMC1716176
- OpenAlex
- W2108136877
- Cited by
- 46
- References
- 30
- Citations by year
- 2026: 1 · 2025: 4 · 2023: 1 · 2021: 1 · 2020: 2 · 2019: 3 · 2018: 1 · 2017: 2 · 2016: 2 · 2015: 3 · 2014: 2 · 2012: 7
- FWCI
- 1.14
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Respiratory Research (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Lund University Publications (Lund University) (submittedVersion)
- Funders
- Lunds Universitet
- Medical Research Council
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- neutrophil phagocytosis, secondary necrosis, neutrophil apoptosis, macrophage clearance, lipopolysaccharide-induced lung inflammation, phagosome, inflammation resolution, neutrophil accumulation
- MeSH terms
- Animals, Female, Lipopolysaccharides, Macrophage Activation, Macrophages, Mice, Inbred BALB C, Neutrophils, Phagocytosis, Pneumonia, Mice
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