HMR 3004对热灭活肺炎链球菌引起的小鼠肺部炎症的免疫调节作用
Immunomodulating effects of HMR 3004 on pulmonary inflammation caused by heat-killed Streptococcus pneumoniae in mice.
作者信息
Duong M, Simard M, Bergeron Y, Ouellet N, Côté-Richer M, Bergeron M G
机构信息
Centre de Recherche en Infectiologie, Centre Hospitalier de l'Université Laval, and Département de Microbiologie, Faculté de Médecine, Université Laval, Québec, Canada G1V 4G2.
出版信息
Antimicrob Agents Chemother. 1998 Dec;42(12):3309-12. doi: 10.1128/AAC.42.12.3309.
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.
摘要
我们研究了新型酮内酯类抗生素HMR 3004对热灭活的异硫氰酸荧光素标记的肺炎链球菌诱导的肺部炎症的影响。HMR 3004下调（P<0.05）了肺炎链球菌诱导的支气管肺泡灌洗液中白细胞介素-6（IL-6）、IL-1β和一氧化氮的释放。该药物限制了（P<0.05）中性粒细胞向肺组织和肺泡的募集，但不干扰吞噬作用。HMR 3004完全消除了肺水肿。通过除具有抗菌特性外还能减轻炎症，HMR 3004可能有助于改善细菌性肺炎的预后。
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