Smoke exposure exacerbates an ethanol-induced defect in mucociliary clearance of Streptococcus pneumoniae.
Smoke exposure exacerbates an ethanol-induced defect in mucociliary clearance of Streptococcus pneumoniae.
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烟雾暴露加剧了乙醇引起的肺炎链球菌粘液纤毛清除缺陷。
DOI：
10.1097/01.alc.0000164364.35682.86
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发表时间：
2005
期刊：
影响因子：
--
通讯作者：
Gentry-Nielsen,MarthaJ
中科院分区：
文献类型：
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作者：
VanderTop,ElizabethA;Wyatt,ToddA;Gentry-Nielsen,MarthaJ
背景酗酒者和吸烟者特别容易受到肺炎链球菌引起的肺部感染。当定植于鼻咽的肺炎球菌被吸入下呼吸道时，感染就开始了。针对这一运动的主要宿主防御是粘液纤毛清除装置。香烟烟雾和乙醇暴露都会改变体外培养的呼吸道粘膜纤毛搏动和蛋白激酶活性，但它们对完整动物体内细菌清除的影响尚未确定。方法雄性SD大鼠连续12周，每天两次暴露于30支香烟产生的烟雾(烟雾暴露)和室内空气(假暴露)。在烟雾暴露的最后五周，大鼠被喂以含有0%、16%、26%或36%乙醇卡路里的Lieber-DeCarli液体饲料。然后，这些大鼠被鼻腔感染了这种病毒。4小时后，通过气管和肺的平板计数来量化细菌进入下呼吸道的数量。每只动物的气管环在β激动剂异丙肾上腺素刺激前和刺激后进行纤毛搏动频率分析，并测定气管上皮细胞蛋白激酶C的活性。肺炎进入大鼠的肺部。虽然单独的烟雾暴露对NS几乎没有影响，但同时吸烟会进一步增加乙醇诱导的缺陷。肺炎运动。吸烟，而不是乙醇暴露，激活了气管上皮细胞PKC。生物进入肺的运动增加与CBF的减少和对异丙肾上腺素的纤毛反应的丧失有关。结论在我们的模型中，摄入EtOH促进了OFS的运动。肺炎进入大鼠的肺部，这种现象因同时暴露在烟雾中而加剧。此外，生物体进入肺部的运动与老鼠对既定刺激的纤毛反应迟钝有关。因此，粘液纤毛清除缺陷可能是酗酒者，特别是吸烟者肺炎球菌感染风险增加的原因之一。
BackgroundAlcoholics and smokers are particularly susceptible to pulmonary infections caused byStreptococcus pneumoniae, the pneumococcus. Infection begins when pneumococci colonizing the nasopharynx are aspirated into the lower respiratory tract. The major host defense against this movement is the mucociliary clearance apparatus. Both cigarette smoke and ethanol (EtOH) exposure alter ciliary beating and protein kinase activity in the respiratory mucosain vitro, but their effects on bacterial clearance in the intact animal have not been determined.MethodsMale Sprague Dawley rats were exposed twice daily for 12 weeks to either the smoke generated from 30 cigarettes (smoke–exposed) or room air (sham–exposed). For the last five weeks of smoke exposure, the rats were fed Lieber‐DeCarli liquid diets containing 0%, 16%, 26%, or 36% EtOH calories. The rats then were infected intranasally withS. pneumoniae, and movement of the organisms into the lower respiratory tract was quantified by plate counts of the tracheas and lungs 4 hr later. Ciliary beat frequency (CBF) analysis was performed on tracheal ring explants from each animal before and after stimulation with the β‐agonist isoproterenol, and tracheal epithelial cell protein kinase C (PKC) activity was measured.ResultsIngestion of any of the EtOH‐containing diets resulted in a dose‐dependent increase in movement ofS. pneumoniaeinto the rats’ lungs. This EtOH‐induced defect was augmented further by concurrent smoke exposure, although smoke exposure alone had little effect onS. pneumoniaemovement. Smoke, but not EtOH exposure, activated tracheal epithelial cell PKC. Increased movement of organisms into lungs correlated with a decrease in CBF and loss of the ciliary response to isoproterenol.ConclusionEtOH ingestion in our model facilitated movement ofS. pneumoniaeinto rats’ lungs, a phenomenon exacerbated by concurrent smoke exposure. Furthermore, the organism's movement into the lungs correlated with a blunting of the rats’ ciliary response to an established stimulus. Defects in mucociliary clearance thus may be one cause of the increased risk of pneumococcal infections in people who abuse alcohol, particularly if they also smoke.