Direct evidence of secondary necrosis of neutrophils during intense lung inflammation.

التفاصيل البيبلوغرافية
العنوان: Direct evidence of secondary necrosis of neutrophils during intense lung inflammation.
المؤلفون: Rydell-Törmänen, Kristina, Uller, Lena, Erjefält, Jonas
المصدر: European Respiratory Journal. 28(2):268-274
مصطلحات موضوعية: lactate dehydrogenase, apoptosis, neutrophils, endotoxin, inflammation, Medicin och hälsovetenskap, Klinisk medicin, Lungmedicin och allergi, Medical and Health Sciences, Clinical Medicine, Respiratory Medicine and Allergy
الوصف: 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.
الوصول الحر: https://lup.lub.lu.se/record/154873Test
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=16510453&dopt=AbstractTest
http://dx.doi.org/10.1183/09031936.06.00126905Test
قاعدة البيانات: SwePub
الوصف
تدمد:13993003
DOI:10.1183/09031936.06.00126905