Type 3 fimbrial shaft (MrkA) of Klebsiella pneumoniae, but not the fimbrial adhesin (MrkD), facilitates biofilm formation
Type 3 fimbrial shaft (MrkA) of Klebsiella pneumoniae, but not the fimbrial adhesin (MrkD), facilitates biofilm formation
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DOI：
10.1128/iai.69.9.5805-5812.2001
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发表时间：
2001-09-01
影响因子：
3.1
通讯作者：
Clegg, S
中科院分区：
文献类型：
--
作者：
Langstraat, J;Bohse, M;Clegg, S
肺炎克雷伯氏菌分离株可引起人类机会性感染，特别是泌尿道和呼吸道感染。这些细菌表达与真核细胞和基质蛋白结合有关的3型菌毛。3型菌毛使用与由MrkA蛋白组成的菌毛轴相关的MrkD粘附素介导与靶组织的结合。研究了克雷伯氏菌在体外形成生物膜的情况。肺炎杆菌的感染表现出受到细菌表面菌毛产生的影响。然而，一个功能性的MrkD粘附素是不必要的有效的生物膜形成。无菌毛菌株形成生物膜的能力受损。本研究利用具有菌毛和无菌毛的克雷伯氏菌等基因系。表达绿色荧光蛋白的肺炎杆菌的结果，可以证明3型菌毛的存在促进了连续流通室中致密生物膜的形成。用具有完整mrk基因簇的质粒转化无菌毛突变体，恢复了菌毛表型和快速形成生物膜的能力。
Isolates of Klebsiella pneumoniae are responsible for opportunistic infections, particularly of the urinary tract and respiratory tract, in humans. These bacteria express type 3 fimbriae that have been implicated in binding to eucaryotic cells and matrix proteins. The type 3 fimbriae mediate binding to target tissue using the MrkD adhesin that is associated with the fimbrial shaft comprised of the MrkA protein. The formation of biofilms in vitro by strains of K. pneumoniae was shown to be affected by the production of fimbriae on the bacterial surface. However, a functional MrkD adhesin was not necessary for efficient biofilm formation. Nonfimbriate strains were impaired in their ability to form biofilms. Using isogenic fimbriate and nonfimbriate strains of K. pneumoniae expressing green fluorescent protein it was possible to demonstrate that the presence of type 3 fimbriae facilitated the formation of dense biofilms in a continuous-flowthrough chamber. Transformation of nonfimbriate mutants with a plasmid possessing an intact mrk gene cluster restored the fimbrial phenotype and the rapid ability to form biofilms.