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Contrasting roles for reactive oxygen species and nitric oxide in the innate response to pulmonary infection with Streptococcus pneumoniae

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Original languageEnglish
Pages (from-to)2485-2490
Number of pages6
JournalVaccine
Volume25
Issue number13
DOIs
Publication statusPublished - 22 Mar 2007
Event5th International Symposium on Pneumococci and Pneumococcal Diseases - Alice Springs, Australia
Duration: 2 Apr 20066 Apr 2006

Abstract

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.

    Research areas

  • macrophages, apoptosis, pneumococci, mice, nitric oxide, ALVEOLAR MACROPHAGES, INDUCED APOPTOSIS, OXIDATIVE STRESS, PHAGOCYTOSIS, CONTRIBUTES, COMMITMENT, ACTIVATION, MECHANISMS, RESISTANCE, CLEARANCE

Event

ID: 17166475