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Immunomodulating effects of HMR 3004 on pulmonary inflammation caused by heat-killed Streptococcus pneumoniae in mice.

Abstract
We investigated the influence of HMR 3004, a new ketolide antibiotic, on the pulmonary inflammation induced by heat-killed fluorescein isothiocyanate-labeled Streptococcus pneumoniae. HMR 3004 downregulated (P < 0.05) the pneumococcus-induced release of interleukin-6 (IL-6), IL-1beta, and nitric oxide in bronchoalveolar lavage fluid. The drug limited (P < 0.05) neutrophil recruitment to lung tissues and alveoli but did not interfere with phagocytosis. HMR 3004 totally abrogated lung edema. By reducing inflammation in addition to possessing antimicrobial properties, HMR 3004 may participate in improving the outcome of bacterial pneumonia.
AuthorsM Duong, M Simard, Y Bergeron, N Ouellet, M Côté-Richer, M G Bergeron
JournalAntimicrobial agents and chemotherapy (Antimicrob Agents Chemother) Vol. 42 Issue 12 Pg. 3309-12 (Dec 1998) ISSN: 0066-4804 [Print] United States
PMID9835535 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Adjuvants, Immunologic
  • Anti-Bacterial Agents
  • Interleukins
  • Ketolides
  • Macrolides
  • RU 64004
  • Tumor Necrosis Factor-alpha
  • Nitric Oxide
Topics
  • Adjuvants, Immunologic (metabolism, pharmacology)
  • Animals
  • Anti-Bacterial Agents (pharmacology)
  • Bronchoalveolar Lavage Fluid (immunology)
  • Inflammation (immunology, metabolism, pathology)
  • Interleukins (metabolism)
  • Ketolides
  • Macrolides
  • Macrophages, Alveolar (drug effects, metabolism)
  • Mice
  • Neutrophils (drug effects, metabolism)
  • Nitric Oxide (metabolism)
  • Streptococcus pneumoniae (immunology)
  • Tumor Necrosis Factor-alpha (metabolism)

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