Entry of Burkholderia organisms into respiratory epithelium: CFTR, microfilament and microtubule dependence.

Entry of Burkholderia organisms into respiratory epithelium: CFTR, microfilament and microtubule dependence.
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DOI:
10.1016/j.jcf.2009.10.002
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发表时间:
2010-01
影响因子:
5.2
通讯作者:
Cannon, Carolyn L.
Cannon, Carolyn L.
中科院分区:
医学2区
文献类型:
--
作者:
Taylor, Jane B.;Hogue, Lisa A.;LiPuma, John J.;Walter, Michael J.;Brody, Steven L.;Cannon, Carolyn L.

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洋葱伯克霍尔德菌复合体(Bcc)感染的发病机制可能与其侵入呼吸道上皮的能力有关。抗生素排除试验用于研究B。dolosa AU 4459和B.新洋葱J2315侵入野生型(WT)和CFTR缺陷型呼吸道上皮细胞。抑制剂用于评估BCC对宿主微管(mt)和微丝(mf)系统的侵袭依赖性。B。dolosa进入WT-CFTR细胞的效率比CFTR缺陷细胞高5倍(分别为25%对5%)。抑制mf或mt后,侵袭率下降至<0.5%。B。cenocepacia以类似的低效率进入WT(0.05%)和CFTR缺陷细胞(0.07%),其在mf或mt抑制下显著降低(分别为0.008%和0.002%)。B。dolosa和B.新洋葱以MF和MT依赖的方式进入呼吸道上皮细胞。突变的CFTR导致B更少的内化。dolosa,但不是B。cenocepacia。
The pathogenesis of infection with Burkholderia cepacia complex (Bcc) organisms may be linked to its capacity to invade respiratory epithelium. An antibiotic exclusion assay was used to study B. dolosa AU4459 and B. cenocepacia J2315 invasion into wild-type (WT) and CFTR-deficient respiratory epithelial cells. Inhibitors were used to evaluate Bcc invasion dependency on host microtubule (mt) and microfilament (mf) systems. B. dolosa entered WT-CFTR cells with 5-fold greater efficiency than CFTR deficient cells (25% vs 5%, respectively). Invasion dropped to <0.5% after either mf or mt inhibition. B. cenocepacia entered WT (0.05%) and CFTR-deficient cells (0.07%) with similarly low efficiencies, which significantly decreased with either mf or mt inhibition (0.008% and 0.002%, respectively). B. dolosa and B. cenocepacia enter respiratory epithelial cells in a mf and mt dependent fashion. Mutated CFTR leads to less internalization of B. dolosa, but not B. cenocepacia.
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