Altered alveolar macrophage function in calorie-restricted rats
Altered alveolar macrophage function in calorie-restricted rats
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DOI：
10.1165/ajrcmb.19.3.3114
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发表时间：
1998-09-01
影响因子：
6.4
通讯作者：
Kari, FW
中科院分区：
文献类型：
--
作者：
Dong, WM;Selgrade, MK;Kari, FW
对雄性Fischer 344大鼠的肺泡巨噬细胞功能进行了评估，这些功能与清除肺部细菌有关，这些大鼠维持在25%卡路里限制的饮食中。限制卡路里摄入和喂食锂盐(对照组)的大鼠暴露在已知会损害肺泡巨噬细胞吞噬功能的臭氧浓度中。臭氧在体外可抑制喂锂大鼠肺泡巨噬细胞对乳胶珠的吞噬作用，但对限制热量的大鼠则无此作用。事实上，卡路里限制增强了对照组和臭氧暴露动物的吞噬功能。自由喂养的臭氧暴露和动物疫链球菌攻击的大鼠经历了多形核白细胞(PMN)的长期感染和内流，而暴露于臭氧的卡路里限制大鼠在24小时内清除了细菌，没有炎症反应。热卡限制大鼠肺泡巨噬细胞在细菌内毒素刺激下，体外产生的一氧化氮和肿瘤坏死因子-α，以及肿瘤坏死因子-α和白介素6信使RNA的表达均较低。总而言之，这些数据表明，限制卡路里摄入增强了对革兰氏阳性细菌的抵抗力，同时降低了内毒素(革兰氏阴性细菌的一种成分)引发的促炎介质的产生。尽管增加细菌耐药性被认为是有益的，但肺诱导炎性介质能力的降低可能会产生积极的和病理生理后果。
Alveolar macrophage functions associated with clearance of bacteria from the lung were assessed in male Fischer 344 rats maintained on a 25% calorie-restricted diet. Calorie-restricted and nd libitum-fed (control) rats were exposed to concentrations of ozone known to compromise phagocytic function of alveolar macrophages. Ozone suppressed alveolar macrophage phagocytosis of latex beads in vitro in nd libitum-fed rats, but not in calorie-restricted rats. In fact, caloric restriction enhanced phagocytic function in both control and ozone-exposed animals. Ad libitum-fed rats exposed to ozone and challenged with Streptococcus zooepidemicus experienced a prolonged infection and influx of polymorphonuclear leukocytes (PMN), whereas calorie-restricted rats exposed to ozone cleared the bacteria in 24 h without an inflammatory response. Bacterial endotoxin-stimulated in vitro production of nitric oxide and tumor necrosis factor (TNF)-alpha as well as expression of TNF-alpha and interleukin-6 messenger RNAs were all lower in alveolar macrophages isolated from calorie-restricted rats. Together, the data suggest that caloric restriction enhances resistance to gram-positive bacteria, while lowering the production of proinflammatory mediators elicited by endotoxin, a component of gram-negative bacteria. Although increased bacterial resistance is considered beneficial, reduction in the lung's ability to induce inflammatory mediators can have both positive and pathophysiologic consequences.