Evidence map›Paper›PMID 21444663›Full record

ArticleInfection and immunity2011

Deletion of mtrC in Haemophilus ducreyi increases sensitivity to human antimicrobial peptides and activates the CpxRA regulon.

Sherri D Rinker, Michael P Trombley, Xiaoping Gu, Kate R Fortney, Margaret E Bauer

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.3field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Interactions of the Skin PathogenFrontiers in immunology · 2020
    Review
  5. Article
  6. Article
  7. Article
  8. ThemBio · 2017
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Sherri D RinkerDepartment of Microbiology and Immunology, Indiana University School of Medicine, 635 Barnhill Drive, Room MS 420, Indianapolis, Indiana 46202-5124, USA.
Michael P Trombley
Xiaoping Gu
Kate R Fortney
Margaret E Bauer
Indiana University School of MedicineIndiana University – Purdue University Indianapolis · US

Funding

University of Washington STI-TM Cooperative Research CtrU19AI031448 · NIAID · UNIVERSITY OF WASHINGTON · PI HOLMES, KING K. · 1995 to 2010
$15.2M
VIRAL DETERMINANTS OF HSV DISEASE IN MICEU19AI031494 · NIAID · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI SPINOLA, STANLEY M. · 1995 to 2009
$13.6M
Immunology and Infectious Diseases Training ProgramT32AI060519 · NIAID · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI MARK H KAPLAN · 2004 to 2026
$6.0M
Training in STIs and infections of global health significanceT32AI007637 · NIAID · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI WOOLS-KALOUSTIAN, KARA KAY · 2001 to 2020
$3.4M
Haemophilus ducreyi Resistance to Antimicrobial PeptidesR21AI075008 · NIAID · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI BAUER, MARGARET E · 2007 to 2008
$412k
UNIVERSITY OF WASHINGTON STD COOPERATIVE RESEARCH CENTERU01AI031448 · NIAID · UNIVERSITY OF WASHINGTON · PI HOLMES, KING KENNARD · 1991 to 1994
–
VARIABILITY IN HERPES SIMPLEX VIRUS GLYCOPROTEINS AND INFECTIVITYU01AI031494 · NIAID · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI BLYTHE, MARGARET J · 1991 to 1994
–
NIAID NIH HHS AI 31448NIAID NIH HHS AI 31494NIAID NIH HHS R21 AI075008NIAID NIH HHS T32 AI007637NIAID NIH HHS T32 AI060519NIAID NIH HHS U19 AI031448NIAID NIH HHS U19 AI031494
6 · The paper itself

Abstract

Haemophilus ducreyi resists killing by antimicrobial peptides encountered during human infection, including cathelicidin LL-37, α-defensins, and β-defensins. In this study, we examined the role of the proton motive force-dependent multiple transferable resistance (MTR) transporter in antimicrobial peptide resistance in H. ducreyi. We found a proton motive force-dependent effect on H. ducreyi's resistance to LL-37 and β-defensin HBD-3, but not α-defensin HNP-2. Deletion of the membrane fusion protein MtrC rendered H. ducreyi more sensitive to LL-37 and human β-defensins but had relatively little effect on α-defensin resistance. The mtrC mutant 35000HPmtrC exhibited phenotypic changes in outer membrane protein profiles, colony morphology, and serum sensitivity, which were restored to wild type by trans-complementation with mtrC. Similar phenotypes were reported in a cpxA mutant; activation of the two-component CpxRA regulator was confirmed by showing transcriptional effects on CpxRA-regulated genes in 35000HPmtrC. A cpxR mutant had wild-type levels of antimicrobial peptide resistance; a cpxA mutation had little effect on defensin resistance but led to increased sensitivity to LL-37. 35000HPmtrC was more sensitive than the cpxA mutant to LL-37, indicating that MTR contributed to LL-37 resistance independent of the CpxRA regulon. The CpxRA regulon did not affect proton motive force-dependent antimicrobial peptide resistance; however, 35000HPmtrC had lost proton motive force-dependent peptide resistance, suggesting that the MTR transporter promotes proton motive force-dependent resistance to LL-37 and human β-defensins. This is the first report of a β-defensin resistance mechanism in H. ducreyi and shows that LL-37 resistance in H. ducreyi is multifactorial.

Indexed as

alpha-DefensinsAntimicrobial Cationic PeptidesBacterial Outer Membrane ProteinsBacterial ProteinsBase Sequencebeta-DefensinsCathelicidinsChancroidGene Expression Regulation, BacterialGenes, BacterialHaemophilus ducreyiHumansMolecular Sequence DataProtein KinasesRegulonReverse Transcriptase Polymerase Chain Reactionalpha-DefensinsAntimicrobial Cationic PeptidesBacterial Outer Membrane ProteinsBacterial Proteinsbeta-DefensinsCathelicidinsCpxA protein, bacteriaCpxR protein, BacteriaProtein Kinases

Identifiers

PMID21444663
PMCPMC3125844
OpenAlexW2139152590

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.