QseC controls biofilm formation of non-typeable Haemophilus influenzae in addition to an AI-2-dependent mechanism

被引：47

作者：

Unal, Can M. ^{[1
]}

Singh, Birendra ^{[1
]}

Fleury, Christophe ^{[1
]}

Singh, Kalpana ^{[1
]}

de Paz, Luis Chavez ^{[2
]}

Svensater, Gunnel ^{[2
]}

Riesbeck, Kristian ^{[1
]}

机构：

[1] Lund Univ, Skane Univ Hosp, Dept Lab Med Malmo, SE-20502 Malmo, Sweden

[2] Malmo Univ, Dept Oral Biol, Malmo, Sweden

来源：

INTERNATIONAL JOURNAL OF MEDICAL MICROBIOLOGY | 2012年 / 302卷 / 06期

基金：

英国医学研究理事会;

关键词：

Biofilm; NTHi; Quorum sensing; Signalling; IN-VITRO; VIRULENCE; IDENTIFICATION; EXACERBATIONS; MATURATION; MANAGEMENT; BACTERIA; PROTEIN; KINASE; ACID;

D O I：

10.1016/j.ijmm.2012.07.013

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

Non-typeable Haemophilus influenzae (NTHi) is a common pathogen associated with diseases such as acute otitis media or exacerbations in patients with chronic obstructive pulmonary disease. The biofilm-forming capability substantially contributes to the persistence of NTHi. However, the regulation of biofilm formation is not completely understood. Quorum sensing regulated by autoinducer-2 produced by luxS is until now the only described regulatory mechanism. In this study, we show that the two-component signalling system QseB/C is involved in the biofilm formation of NTHi in vitro. An isogenic NTHi mutant of qseC (Hi3655KR2) showed a significant decrease in biofilm formation under static and semi-static conditions as assessed by crystal violet staining. In addition, under constant flow conditions, Hi3655KR2 formed less biofilm after 48 h. The biofilm defects were irrespective of autoinducer-2 levels. Hence, here we suggest for the first time a regulatory circuit in NTHi, which controls biofilm formation by mechanisms other than or in addition to luxS-dependent factors. (c) 2012 Elsevier GmbH. All rights reserved.

引用

页码：261 / 269

页数：9

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