Modulation of epithelial sodium channel (ENaC) expression in mouse lung infected with Pseudomonas aeruginosa.

Modulation of epithelial sodium channel (ENaC) expression in mouse lung infected with Pseudomonas aeruginosa.
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DOI:
10.1186/1465-9921-6-2
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发表时间:
2005-01-06
影响因子:
5.8
通讯作者:
Berthiaume Y
Berthiaume Y
中科院分区:
医学2区
文献类型:
--
作者:
Dagenais A;Gosselin D;Guilbault C;Radzioch D;Berthiaume Y

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将包埋在琼脂珠中的铜绿假单胞菌气管内滴注到小鼠肺中,导致易感小鼠品系的慢性肺部感染。由于感染产生强烈的炎症反应并伴有一定程度的肺水肿,我们测试了它是否可以调节参与肺液体清除的基因的表达,例如上皮钠通道(ENaC)的α、β和γ亚基以及Na+-K+-ATP酶的催化亚基。将包埋在琼脂珠中的铜绿假单胞菌滴入耐药(BalB/c)和敏感(DBA/2、C57 BL/6和A/J)小鼠品系的肺部。用北方印迹法检测感染后3 h ~ 14 d肺组织中ENaC和Na+-K+-ATP酶亚基mRNA的表达。不同小鼠品系的感染引起α和β ENaC mRNA的调节。假单胞菌感染后,αENaC mRNA的表达在感染后第3天和第7天下降至中位数43%,在感染后第14天仍下降至中位数45%(p < 0.05)。βENaC mRNA的相对表达在感染后24 h短暂增加至241%的中位数,然后在感染后第3天和第7天下降至对照的43%和54%的中位数(p < 0.05)。尽管γENaC亚基的表达模式与α和β亚基相似,但未检测到γENaC mRNA的显著调节。没有记录到钠泵催化亚基α 1 Na +-K+-ATP酶mRNA的调节。这三个亚基的独特表达谱在易感和耐药小鼠品系之间没有差异。这些结果表明,假单胞菌感染,通过调节ENaC亚基的表达,可以影响水肿的形成和清除感染的肺。
The intratracheal instillation of Pseudomonas aeruginosa entrapped in agar beads in the mouse lung leads to chronic lung infection in susceptible mouse strains. As the infection generates a strong inflammatory response with some lung edema, we tested if it could modulate the expression of genes involved in lung liquid clearance, such as the α, β and γ subunits of the epithelial sodium channel (ENaC) and the catalytic subunit of Na+-K+-ATPase. Pseudomonas aeruginosa entrapped in agar beads were instilled in the lung of resistant (BalB/c) and susceptible (DBA/2, C57BL/6 and A/J) mouse strains. The mRNA expression of ENaC and Na+-K+-ATPase subunits was tested in the lung by Northern blot following a 3 hours to 14 days infection. The infection of the different mouse strains evoked regulation of α and β ENaC mRNA. Following Pseudomonas instillation, the expression of αENaC mRNA decreased to a median of 43% on days 3 and 7 after infection and was still decreased to a median of 45% 14 days after infection (p < 0.05). The relative expression of βENaC mRNA was transiently increased to a median of 241%, 24 h post-infection before decreasing to a median of 43% and 54% of control on days 3 and 7 post-infection (p < 0.05). No significant modulation of γENaC mRNA was detected although the general pattern of expression of the subunit was similar to α and β subunits. No modulation of α1Na+-K+-ATPase mRNA, the catalytic subunit of the sodium pump, was recorded. The distinctive expression profiles of the three subunits were not different, between the susceptible and resistant mouse strains. These results show that Pseudomonas infection, by modulating ENaC subunit expression, could influence edema formation and clearance in infected lungs.
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