Long-chain polyunsaturated fatty acids modulate lung inflammatory response induced by Pseudomonas aeruginosa in mice
Long-chain polyunsaturated fatty acids modulate lung inflammatory response induced by Pseudomonas aeruginosa in mice
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DOI：
10.1203/01.pdr.0000169979.27641.40
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发表时间：
2005-08-01
影响因子：
3.6
通讯作者：
Guery, BP
中科院分区：
文献类型：
--
作者：
Auvin, S;Collet, FS;Guery, BP
多不饱和脂肪酸（PUFA）在慢性感染中的免疫调节特性已被广泛研究。很少有研究关注急性感染；因此，我们评估了PUFA在铜绿假单胞菌（PA）诱导的肺损伤小鼠模型中的作用。将C57BL/6小鼠随机分为二十碳五烯酸（EPA）饲粮、花生四烯酸（AA）饲粮和对照饲粮（饱和脂肪酸）喂养3周。每只小鼠气管内灌注10(7)CFU PA诱导肺损伤。在每个饮食组中，分别对pa诱导的肺损伤进行研究。评价标准为早期死亡率；用支气管肺泡灌洗液中肿瘤坏死因子- α (tnf - α)、IL-1 β、IL-6和IL-10水平评估炎症反应；肺损伤评估；伤后24小时肺血管外积水。pa诱导肺损伤后，早期死亡率无差异；EPA饮食组的tnf -水平明显高于其他两个饮食组。其他细胞因子在两组之间没有差异。在EPA组中，肺水肿也更为重要，这与tnf - α水平的变化一致。我们的研究清楚地表明，在pa诱导的急性肺损伤中，n-3 PUFA诱导了炎症反应的差异，并伴有较高程度的肺水肿。用n-3 PUFA调节炎症反应可以影响对细菌攻击的反应。
Polyunsaturated fatty acid (PUFA) immunomodulatory properties have been studied extensively in chronic infections. Few studies have focused on acute infection; thus, PUFA effects in a mouse model of Pseudomonas aeruginosa (PA)-induced lung injury were evaluated. C57BL/6 mice were randomized to be fed for 3 wk with an eicosapentaenoic acid (EPA) diet, an arachidonic acid (AA) diet, or a control diet [saturated fatty acids]. Lung injury was induced by intratracheal instillation of 10(7) CFU of PA per mouse. In each diet group, animals were studied either without or after PA-inducing lung injury. Evaluation criteria were early mortality; inflammatory response assessed with tumor necrosis factor-alpha (TNF-alpha), IL-1 beta, IL-6 and IL-10 levels in bronchoalveolar lavage; lung injury evaluation; and extravascular lung water, assessed 24 h after the injury. After PA-induced lung injury, no difference in early mortality was observed; TNF-alpha level was significantly higher in the EPA diet than in the other two diet groups. No difference for the other cytokines was found among the groups. Lung edema was also more important in the EPA group, consistent with the variations of TNF-alpha levels. Our study clearly shows that in PA-induced acute lung injury, n-3 PUFA induces differences in the inflammatory response with a higher level of lung edema. Modulation of the inflammatory response with n-3 PUFA can influence the response to a bacterial challenge.