Direct evidence of secondary necrosis of neutrophils during intense lung inflammation.
Rydell-Törmänen, Kristina LU
; Uller, Lena
LU
and Erjefält, Jonas
LU
(2006)
In European Respiratory Journal
28(2).
p.268-274
- Abstract
- Several pulmonary inflammatory conditions are characterised by infiltration of neutrophils. Normally, neutrophils are silently removed by apoptosis, followed by phagocytosis. However, if phagocytosis fails, apoptotic cells undergo secondary necrosis. Recent findings of increased levels of the pan-necrosis marker lactate dehydrogenase in bronchoalveolar lavage from lipopolysaccharide-exposed mice implies potential involvement of secondary necrosis. Using a similar model, this study aimed to identify the source of lactate dehydrogenase and to search for direct histological evidence of secondary necrosis. Lipopolysaccharide (LPS) was administered to the lungs of BALB/c mice, and bronchoalveolar lavage and tissue samples were collected 4, 12,... (More)
- Several pulmonary inflammatory conditions are characterised by infiltration of neutrophils. Normally, neutrophils are silently removed by apoptosis, followed by phagocytosis. However, if phagocytosis fails, apoptotic cells undergo secondary necrosis. Recent findings of increased levels of the pan-necrosis marker lactate dehydrogenase in bronchoalveolar lavage from lipopolysaccharide-exposed mice implies potential involvement of secondary necrosis. Using a similar model, this study aimed to identify the source of lactate dehydrogenase and to search for direct histological evidence of secondary necrosis. Lipopolysaccharide (LPS) was administered to the lungs of BALB/c mice, and bronchoalveolar lavage and tissue samples were collected 4, 12, 24, 36, 48, 60 and 72 h after administration. LPS induced a patchy neutrophil-rich lung inflammation, where the numbers of terminal deoxynucleotide transferase-mediated dUTP nick-end labeling-positive neutrophils were increased at 12 h and onwards. Lavage levels of neutrophils and lactate dehydrogenase increased significantly at 4 and 24 h, respectively. Detailed electron microscopic assessment of neutrophil activation and death modes revealed that up to 14% of the neutrophils were undergoing secondary necrosis, whereas apoptotic or primary necrotic structural cells were rarely found. In summary, this study provides direct evidence that secondary necrosis of neutrophils is a common process during intense lung inflammation. This implies that neutrophil apoptosis may cause rather than resolve airway inflammation. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/154873
- author
- Rydell-Törmänen, Kristina
LU
; Uller, Lena
LU
and Erjefält, Jonas
LU
- organization
- publishing date
- 2006
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- lactate dehydrogenase, apoptosis, neutrophils, endotoxin, inflammation
- in
- European Respiratory Journal
- volume
- 28
- issue
- 2
- pages
- 268 - 274
- publisher
- European Respiratory Society
- external identifiers
-
- wos:000239525000005
- scopus:33845478130
- pmid:16510453
- ISSN
- 1399-3003
- DOI
- 10.1183/09031936.06.00126905
- language
- English
- LU publication?
- yes
- id
- ffef76f8-8ccb-4eb1-8837-18e1d97da6c7 (old id 154873)
- alternative location
- http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=16510453&dopt=Abstract
- date added to LUP
- 2016-04-01 12:35:30
- date last changed
- 2022-04-06 00:27:20
@article{ffef76f8-8ccb-4eb1-8837-18e1d97da6c7,
abstract = {{Several pulmonary inflammatory conditions are characterised by infiltration of neutrophils. Normally, neutrophils are silently removed by apoptosis, followed by phagocytosis. However, if phagocytosis fails, apoptotic cells undergo secondary necrosis. Recent findings of increased levels of the pan-necrosis marker lactate dehydrogenase in bronchoalveolar lavage from lipopolysaccharide-exposed mice implies potential involvement of secondary necrosis. Using a similar model, this study aimed to identify the source of lactate dehydrogenase and to search for direct histological evidence of secondary necrosis. Lipopolysaccharide (LPS) was administered to the lungs of BALB/c mice, and bronchoalveolar lavage and tissue samples were collected 4, 12, 24, 36, 48, 60 and 72 h after administration. LPS induced a patchy neutrophil-rich lung inflammation, where the numbers of terminal deoxynucleotide transferase-mediated dUTP nick-end labeling-positive neutrophils were increased at 12 h and onwards. Lavage levels of neutrophils and lactate dehydrogenase increased significantly at 4 and 24 h, respectively. Detailed electron microscopic assessment of neutrophil activation and death modes revealed that up to 14% of the neutrophils were undergoing secondary necrosis, whereas apoptotic or primary necrotic structural cells were rarely found. In summary, this study provides direct evidence that secondary necrosis of neutrophils is a common process during intense lung inflammation. This implies that neutrophil apoptosis may cause rather than resolve airway inflammation.}},
author = {{Rydell-Törmänen, Kristina and Uller, Lena and Erjefält, Jonas}},
issn = {{1399-3003}},
keywords = {{lactate dehydrogenase; apoptosis; neutrophils; endotoxin; inflammation}},
language = {{eng}},
number = {{2}},
pages = {{268--274}},
publisher = {{European Respiratory Society}},
series = {{European Respiratory Journal}},
title = {{Direct evidence of secondary necrosis of neutrophils during intense lung inflammation.}},
url = {{http://dx.doi.org/10.1183/09031936.06.00126905}},
doi = {{10.1183/09031936.06.00126905}},
volume = {{28}},
year = {{2006}},
}