Influence of cefodizime on pulmonary inflammatory response to heat-killed Klebsiella pneumoniae in mice
Influence of cefodizime on pulmonary inflammatory response to heat-killed Klebsiella pneumoniae in mice
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DOI：
10.1128/aac.43.9.2291
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发表时间：
1999-09-01
影响因子：
4.9
通讯作者：
Bergeron, MG
中科院分区：
文献类型：
--
作者：
Bergeron, Y;Deslauriers, AM;Bergeron, MG
包封的肺炎克雷伯菌菌株经常诱发致命的医院获得性肺炎。头孢地嗪（CEF）作为一种抗生素，被怀疑通过与细菌和宿主细胞的相互作用来增强宿主对各种微生物入侵的抗性。为了研究CEF对克雷伯氏菌肺部反应的影响，而不仅仅是由药物直接清除细菌引起的，我们用热灭活的异硫氰酸荧光素标记的肺炎克雷伯氏菌接种小鼠。CEF能显著上调克雷伯菌诱导的早期肺泡巨噬细胞分泌肿瘤坏死因子α（TNF α）（P < 0.01），并能显著上调肺泡巨噬细胞数量（P < 0.01）和吞噬功能（P < 0.001）。与此相反，晚期中性粒细胞聚集（P < 0.05）和白细胞介素-1 α（IL-1 α）（P < 0.05）和IL-6（P < 0.05）水平降低。CEF刺激早期免疫反应，随后减少炎症，可能对细菌性肺炎有益。
Encapsulated Klebsiella pneumoniae strains frequently induce fatal nosocomial pneumonia. Cefodizime (CEF) as an antibiotic is suspected to enhance host resistance against various microbial invasions through interactions with bacteria and host cells. To investigate the influence of CEF on the pulmonary response to Klebsiella that does not merely result from direct bacterial clearance by the drug, we inoculated mice with heat-killed fluorescein isothiocyanate-labeled K: pneumoniae. CEF upregulated (P < 0.01) the early Klebsiella-induced secretion of tumor necrosis factor alpha, as well as the number (P < 0.01) and phagocytic efficacy (P < 0.001) of alveolar macrophages. By contrast, the late polymorphonuclear neutrophil recruitment (P < 0.05) and levels of interleukin-1 alpha (IL-1 alpha) (P < 0.05) and IL-6 (P < 0.05) were reduced. The stimulation of an early immune response by CEF followed by late reduction in inflammation may be beneficial against bacterial pneumonia.