Actinobacillus pleuropneumoniae two-component system QseB/QseC regulates the transcription of PilM, an important determinant of bacterial adherence and virulence

Liu, Jinlin; Hu, Linlin; Zhao, Xu; Tan, Chen; Yuan, Fangyan; Fu, Shulin; Cheng, Hui; Chen, Huanchun; Bei, Weicheng

doi:10.1016/j.vetmic.2015.02.033

Cited by 31 publications

(24 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Similar to A. actinomycetemcomitans , expression of the qseBC operon in Actinobacillus pleuropneumoniae is induced by both Ep and Ne (Li et al ., ) and catecholamines induce several other virulence factors as well, including apxlA (encoding a toxin in the RTX family), pgaB (production of extracellular matrix carbohydrate) and APL_0443 (autotransporter adhesion). Inactivation of the qseBC operon also resulted in reduced expression of 17 Actinobacillus pleuropneumoniae genes including hugZ , encoding a putative heme/iron utilization protein, and pilM encoding a Tfp pilus assembly protein (Liu et al ., ). PilM mediates adherence of Actinobacillus pleuropneumoniae to porcine lung cells and QseB was shown to directly bind to the pilM promoter (Liu et al ., ).…”

Section: Functional Outcomes Of Qsebc Activation: Biofilms and Virulencementioning

confidence: 97%

“…Inactivation of the qseBC operon also resulted in reduced expression of 17 Actinobacillus pleuropneumoniae genes including hugZ , encoding a putative heme/iron utilization protein, and pilM encoding a Tfp pilus assembly protein (Liu et al ., ). PilM mediates adherence of Actinobacillus pleuropneumoniae to porcine lung cells and QseB was shown to directly bind to the pilM promoter (Liu et al ., ). However, following intratracheal challenge, virulence of the Δ qseBC mutant did not significantly differ from wild‐type in a porcine pneumonia model (Liu et al ., ).…”

Section: Functional Outcomes Of Qsebc Activation: Biofilms and Virulencementioning

confidence: 97%

“…PilM mediates adherence of Actinobacillus pleuropneumoniae to porcine lung cells and QseB was shown to directly bind to the pilM promoter (Liu et al ., ). However, following intratracheal challenge, virulence of the Δ qseBC mutant did not significantly differ from wild‐type in a porcine pneumonia model (Liu et al ., ). Interestingly, although pilM expression is reduced in the Δ qseBC strain, deletion of pilM resulted in a significant attenuation of virulence.…”

Section: Functional Outcomes Of Qsebc Activation: Biofilms and Virulencementioning

confidence: 97%

See 2 more Smart Citations

QseBC, a two‐component bacterial adrenergic receptor and global regulator of virulence in Enterobacteriaceae and Pasteurellaceae

Weigel

Demuth

2015

Molecular Oral Microbiology

View full text Add to dashboard Cite

SummaryThe QseBC two‐component system (TCS) is associated with quorum sensing and functions as a global regulator of virulence. Based on sequence similarity within the sensor domain and conservation of an acidic motif essential for signal recognition, QseBC is primarily distributed in the Enterobacteriaceae and Pasteurellaceae. In Escherichia coli, QseC responds to autoinducer‐3 and/or epinephrine/norepinephrine. Binding of epinephrine/norepinephrine is inhibited by adrenergic antagonists; hence QseC functions as a bacterial adrenergic receptor. Aggregatibacter actinomycetemcomitans QseC is activated by a combination of epinephrine/norepinephrine and iron, whereas only iron activates the Haemophilus influenzae sensor. QseC phosphorylates QseB but there is growing evidence that QseB is activated by non‐cognate sensors and regulated by dephosphorylation via QseC. Interestingly, the QseBC signaling cascades and regulons differ significantly. In enterohemorrhagic E. coli, QseC induces expression of a second adrenergic TCS and phosphorylates two non‐cognate response regulators, each of which induces specific sets of virulence genes. This signaling pathway integrates with other regulatory mechanisms mediated by transcriptional regulators QseA and QseD and a fucose‐sensing TCS and likely controls the level and timing of virulence gene expression. In contrast, A. actinomycetemcomitans QseC signals through QseB to regulate genes involved in anaerobic metabolism and energy production, which may prime cellular metabolism for growth in an anaerobic host niche. QseC represents a novel target for therapeutic intervention and small molecule inhibitors already show promise as broad‐spectrum antimicrobials. Further characterization of QseBC signaling may identify additional differences in QseBC function and inform further development of new therapeutics to control microbial infections.

show abstract

Section: Functional Outcomes Of Qsebc Activation: Biofilms and Virulencementioning

confidence: 97%

Section: Functional Outcomes Of Qsebc Activation: Biofilms and Virulencementioning

confidence: 97%

Section: Functional Outcomes Of Qsebc Activation: Biofilms and Virulencementioning

confidence: 97%

See 1 more Smart Citation

QseBC, a two‐component bacterial adrenergic receptor and global regulator of virulence in Enterobacteriaceae and Pasteurellaceae

Weigel

Demuth

2015

Molecular Oral Microbiology

View full text Add to dashboard Cite

show abstract

“…The two-component signal transduction systems function in response to prokaryotes under a variety of external conditions. It was uncovered that a total of 48 two-component systems (TCS) exist in the genome of strain J-5, including ComP/ComA (10) DegS/DegV (11), QseC/QseB (12), PhoR/PhoP (13), and DesK/DesR (14). The genes encoding RpoS and RpoN (15), which play roles in bacterial adaptation to environmental stress, were also identified in the genome of this strain.…”

Section: Genome Announcementmentioning

confidence: 99%

Complete Genome Sequence of Bacillus subtilis J-5, a Potential Biocontrol Agent

et al. 2017

View full text Add to dashboard Cite

show abstract

“…Manuscript to be reviewed MG1655 (Clarke & Sperandio 2005b;Gou et al 2019), bacterial adherence in Actinobacillus pleuropneumoniae (Liu et al 2015) and biofilm formation in Aggregatibacter actinomycetemcomitans (Juarez-Rodriguez et al 2013). However, whether QseBC regulate the antibiotic susceptibility and biofilm formation in E. coli strain isolated from bovine mastitis has not been reported.…”

Section: Introductionmentioning

confidence: 99%

Peer Review #2 of "QseBC is involved in the biofilm formation and antibiotic resistance in Escherichia coli isolated from bovine mastitis (v0.1)"

2020

View full text Add to dashboard Cite

Background Mastitis is one of the most common infectious diseases in dairy cattle and causes significant financial losses in the dairy industry worldwide. Antibiotic therapy has been used as the most effective strategy for clinical mastitis treatment. However, due to the extensive use of antibacterial agents, antimicrobial resistance (AMR) is considered to be one of the reasons for low cure rates in bovine mastitis. In addition, biofilms could protect bacteria by restricting antibiotic access and shielding the bacterial pathogen from mammary gland immune defences. The functional mechanisms of quorum sensing E. coli regulators B an d C (QseBC) have been well studied in E. coli model strains; however, whether QseBC regulates antibiotic susceptibility and biofilm formation in clinical E. coli strain has not been reported. Methods In this study, we performed construction of the qseBC gene mutant, complementation of the qseBC mutant, antimicrobial susceptibility testing, antibacterial activity assays, biofilm formation assays, realtime reverse transcription PCR (RT-PCR) experiments and electrophoretic mobility shift assays (EMSAs) to investigate the role of qseBC in regulating biofilm formation and antibiotic susceptibility in the clinical E. coli strain ECDCM2. Results We reported that inactivation of QseBC led to a decrease in biofilm formation capacity and an increase in antibiotic susceptibility of an E. coli strain isolated from a dairy cow that suffered from mastitis. In addition, this study indicated that QseBC increased biofilm formation by upregulating the transcription of the biofilm-associated genes bcsA, csgA, fliC, motA, wcaF and fimA and decreased antibiotic susceptibility by upregulating the transcription of the efflux-pump-associated genes marA, acrA, acrB, acrD, emrD and mdtH. We also performed EMSA assays, and the results showed that QseB can directly bind to the marA promoter. Conclusions The QseBC two-component system affects antibiotic sensitivity by regulating the transcription of effluxpump-associated genes. Further, biofilm-formation-associated genes were also regulated by QseBC TCS in E. coli ECDCM2. Hence, this study might provide new clues to the prevention and treatment of infections caused by the clinical E. coli strains.

show abstract

Actinobacillus pleuropneumoniae two-component system QseB/QseC regulates the transcription of PilM, an important determinant of bacterial adherence and virulence

Cited by 31 publications

References 34 publications

QseBC, a two‐component bacterial adrenergic receptor and global regulator of virulence in Enterobacteriaceae and Pasteurellaceae

QseBC, a two‐component bacterial adrenergic receptor and global regulator of virulence in Enterobacteriaceae and Pasteurellaceae

Complete Genome Sequence of Bacillus subtilis J-5, a Potential Biocontrol Agent

Peer Review #2 of "QseBC is involved in the biofilm formation and antibiotic resistance in Escherichia coli isolated from bovine mastitis (v0.1)"

Contact Info

Product

Resources

About