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

Helen M. Marriott, Paul G. Hellewell, Moira K. B. Whyte, David Dockrell

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

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.

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

Keywords / Materials (for Non-textual outputs)

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

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