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Cited by 890

The DOI matches its Crossref record; 48 of the 48 references it cites were found in a registry or an index.

Excessive Neutrophils and Neutrophil Extracellular Traps Contribute to Acute Lung Injury of Influenza Pneumonitis

Open access
Narasaraju, Teluguakula, Yang, Edwin, Samy, Ramar Perumal, Ng, Huey Hian, Poh, Wee Peng, Liew, Audrey-Ann, Phoon, Meng Chee, van Rooijen, Nico, Chow, Vincent T.·2011·The American Journal of Pathology
DOI 10.1016/j.ajpath.2011.03.013
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Abstract

Complications of acute respiratory distress syndrome (ARDS) are common among critically ill patients infected with highly pathogenic influenza viruses. Macrophages and neutrophils constitute the majority of cells recruited into infected lungs, and are associated with immunopathology in influenza pneumonia. We examined pathological manifestations in models of macrophage- or neutrophil-depleted mice challenged with sublethal doses of influenza A virus H1N1 strain PR8. Infected mice depleted of macrophages displayed excessive neutrophilic infiltration, alveolar damage, and increased viral load, later progressing into ARDS-like pathological signs with diffuse alveolar damage, pulmonary edema, hemorrhage, and hypoxemia. In contrast, neutrophil-depleted animals showed mild pathology in lungs. The brochoalveolar lavage fluid of infected macrophage-depleted mice exhibited elevated protein content, T1-α, thrombomodulin, matrix metalloproteinase-9, and myeloperoxidase activities indicating augmented alveolar-capillary damage, compared to neutrophil-depleted animals. We provide evidence for the formation of neutrophil extracellular traps (NETs), entangled with alveoli in areas of tissue injury, suggesting their potential link with lung damage. When co-incubated with infected alveolar epithelial cells in vitro, neutrophils from infected lungs strongly induced NETs generation, and augmented endothelial damage. NETs induction was abrogated by anti-myeloperoxidase antibody and an inhibitor of superoxide dismutase, thus implying that NETs generation is induced by redox enzymes in influenza pneumonia. These findings support the pathogenic effects of excessive neutrophils in acute lung injury of influenza pneumonia by instigating alveolar-capillary damage.

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Crossref · 10.1016/j.ajpath.2011.03.013

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Metadata

Authors
Narasaraju, T., Yang, E., Samy, R. P., Ng, H. H., Poh, W. P., Liew, A.-A., Phoon, M. C., van Rooijen, N., & Chow, V. T.
Venue
The American Journal of Pathology
Publisher
Elsevier BV
Published
2011-07
Volume
179
Issue
1
Pages
199-210
ISSN
0002-9440 (ISSN-L)
DOI
10.1016/j.ajpath.2011.03.013
OpenAlex
W2129339954
Cited by
890
References
48
FWCI
13.50
Type
journal article
Language
en
Open access
bronze

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