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Respiratory syncytial virus increases eosinophil extracellular traps in a murine model of asthma
Respiratory viral infections are the leading cause of asthma exacerbations. Eosinophil activation results in the formation of eosinophil extracellular traps (EETs), which release web-like structures of DNA and proteins that bind, disarm and extracellularly kill pathogens. We investigated whether the...
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Published in: | Asia Pacific allergy 2019-10, Vol.9 (4), p.e32-e32 |
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Main Authors: | , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that cite this one |
Online Access: | Get full text |
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Summary: | Respiratory viral infections are the leading cause of asthma exacerbations. Eosinophil activation results in the formation of eosinophil extracellular traps (EETs), which release web-like structures of DNA and proteins that bind, disarm and extracellularly kill pathogens.
We investigated whether the respiratory syncytial virus (RSV)
could induce EETs in bronchoalveolar lavage fluid eosinophils in a murine model of asthma.
BALB/cJ mice (6-8 weeks old) were sensitized with 2 subcutaneous injections of ovalbumin (20 μg) on days 0 and 7, followed by three intranasal challenges with ovalbumin (100 μg) on days 14, 15, and 16 of the protocol. The control group received Dulbecco's phosphate-buffered saline. Bronchoalveolar lavage fluid eosinophils of ovalbumin group or control group were stimulated with RSV (10
PFU/mL)
for 3 hours. After that, culture supernatant was collected to perform the analyses proposed in this study.
We verified an increase in extracellular DNA concentration in bronchoalveolar lavage fluid eosinophils from ovalbumin group stimulated with RSV (10
PFU/mL)
, which was confirmed by confocal microscopy. We demonstrated that most cells are negative for annexin V and propidium iodide in all groups evaluated. Also, RSV
decreased interferon-ɣ in culture supernatant when compared to the ovalbumin group.
In this study, we demonstrated for the first time that RSV
induces EETs formation in eosinophils from asthmatic mice. |
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ISSN: | 2233-8276 2233-8268 |
DOI: | 10.5415/apallergy.2019.9.e32 |