Martin T R, Altman L C, Alvares O F
Am Rev Respir Dis. 1983 Dec;128(6):1013-9. doi: 10.1164/arrd.1983.128.6.1013.
Protein-calorie malnutrition (PCM) impairs systemic immunity in humans and animals, but its effects on regional defense mechanisms in the lung are not clear. Therefore, we investigated lung phagocytic antibacterial defenses in vivo and in vitro in an animal model of PCM. Matched groups of weanling rats consumed Isocaloric diets containing either 0.8% (PCM) or 24% protein (Control, C). A third group of animals was fed the C diet in restricted amounts to match the daily caloric intake of the PCM animals (pair-fed control, PF). After 4 wk on the diet, PCM animals were hypoproteinemic, hypoalbuminemic, and anemic and had depressed systemic cell-mediated immunity. In vivo, the lung clearance rate of Listeria monocytogenes was markedly delayed in PCM animals (% bacterial recovery at 9 days, mean +/- SE:PCM = 120 +/- 25.1; PF = 5.2 +/- 3.0; C = 0.6 +/- 0.6; p less than 0.001 for PCM versus C). Only 36% of the PCM animals survived for 9 days after Listeria exposure, whereas more than 94% of the C and PF animals survived (p less than 0.01). Recruitment of macrophages to the lungs of PCM animals after Listeria aerosolization was markedly impaired compared with that in the PF and C animals (p less than 0.001). By contrast, lung clearance rates of 2 pyogenic organisms, Staphylococcus aureus 502a and Pseudomonas aeruginosa 177, were similar in all groups. In vitro, alveolar macrophage chemotaxis toward zymosan-activated serum, and microbicidal activity against Staphylococcus epidermidis were also similar in all groups of animals. Our findings indicate that in the rat, PCM impairs the pulmonary clearance of L. monocytogenes, and that this defect is associated with impaired macrophage recruitment to the lung after Listeria inhalation.(ABSTRACT TRUNCATED AT 250 WORDS)
蛋白质 - 热量营养不良(PCM)会损害人类和动物的全身免疫力,但其对肺部局部防御机制的影响尚不清楚。因此,我们在PCM动物模型中对肺部吞噬细胞的抗菌防御进行了体内和体外研究。将断奶大鼠分成匹配组,分别给予含0.8%蛋白质的等热量饮食(PCM组)或含24%蛋白质的饮食(对照组,C组)。第三组动物给予C组饮食,但限制量以匹配PCM组动物的每日热量摄入(配对喂养对照组,PF组)。饮食4周后,PCM组动物出现低蛋白血症、低白蛋白血症和贫血,全身细胞介导的免疫功能受到抑制。在体内,PCM组动物对单核细胞增生李斯特菌的肺部清除率明显延迟(9天时细菌回收率,平均值±标准误:PCM组 = 120 ± 25.1;PF组 = 5.2 ± 3.0;C组 = 0.6 ± 0.6;PCM组与C组相比,p < 0.001)。暴露于李斯特菌后,只有36%的PCM组动物存活9天,而C组和PF组超过94%的动物存活(p < 0.01)。与PF组和C组动物相比,PCM组动物雾化吸入李斯特菌后巨噬细胞向肺部的募集明显受损(p < 0.001)。相比之下,所有组对两种化脓性微生物金黄色葡萄球菌502a和铜绿假单胞菌177的肺部清除率相似。在体外,所有组动物肺泡巨噬细胞对酵母聚糖激活血清的趋化性以及对表皮葡萄球菌的杀菌活性也相似。我们的研究结果表明,在大鼠中,PCM会损害肺部对单核细胞增生李斯特菌的清除,并且这种缺陷与吸入李斯特菌后巨噬细胞向肺部的募集受损有关。(摘要截短至250字)