Research output: Contribution to journal › Article › peer-review
Original language | English |
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Pages (from-to) | 2485-2490 |
Number of pages | 6 |
Journal | Vaccine |
Volume | 25 |
Issue number | 13 |
DOIs | |
Publication status | Published - 22 Mar 2007 |
Event | 5th International Symposium on Pneumococci and Pneumococcal Diseases - Alice Springs, Australia Duration: 2 Apr 2006 → 6 Apr 2006 |
The pulmonary innate response to low-dose bacterial challenge requires functioning alveolar macrophages (AM) but also subsequent macrophage apoptosis. To address the role of reactive oxygen species (ROS) and nitric oxide (NO) in AM apoptosis, sub-clinical Streptococcus pneumoniae infection was established in gp91(phox-/-) and inducible NO synthase deficient (iNOS(-/-)) mice. Both AM apoptosis and the number of macrophages containing apoptotic bodies are reduced in iNOS(-/-) as compared to control or gp91phox(-/-) mice. iNOS(-/-) mice recruit neutrophils and generate TNF-alpha to compensate for impaired AM competence but ROS deficiency has no apparent effect on AM function in this model. (C) 2006 Elsevier Ltd. All rights reserved.
2/04/06 → 6/04/06
AustraliaEvent: Conference
ID: 17166475