Inhibitors of Pathogen Intercellular Signals as Selective Anti-Infective Compounds
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{"title"=>"Inhibitors of pathogen intercellular signals as selective anti-infective compounds", "type"=>"journal", "authors"=>[{"first_name"=>"Biliana", "last_name"=>"Lesic", "scopus_author_id"=>"15074166900"}, {"first_name"=>"François", "last_name"=>"Lépine", "scopus_author_id"=>"7006611357"}, {"first_name"=>"Eric", "last_name"=>"Déziel", "scopus_author_id"=>"6602634781"}, {"first_name"=>"Jiangwen", "last_name"=>"Zhang", "scopus_author_id"=>"22137260600"}, {"first_name"=>"Qunhao", "last_name"=>"Zhang", "scopus_author_id"=>"8558801500"}, {"first_name"=>"Katie", "last_name"=>"Padfield", "scopus_author_id"=>"8558801400"}, {"first_name"=>"Marie Hélène", "last_name"=>"Castonguay", "scopus_author_id"=>"15074123400"}, {"first_name"=>"Sylvain", "last_name"=>"Milot", "scopus_author_id"=>"6603387958"}, {"first_name"=>"Scott", "last_name"=>"Stachel", "scopus_author_id"=>"57189215498"}, {"first_name"=>"A. Aria", "last_name"=>"Tzika", "scopus_author_id"=>"7003635500"}, {"first_name"=>"Ronald G.", "last_name"=>"Tompkins", "scopus_author_id"=>"7101805272"}, {"first_name"=>"Laurence G.", "last_name"=>"Rahme", "scopus_author_id"=>"6603919311"}], "year"=>2007, "source"=>"PLoS Pathogens", "identifiers"=>{"scopus"=>"2-s2.0-34848815010", "sgr"=>"34848815010", "issn"=>"15537366", "doi"=>"10.1371/journal.ppat.0030126", "pmid"=>"17941706", "isbn"=>"1553-7374 (Electronic)\\r1553-7366 (Linking)", "pui"=>"47510276"}, "id"=>"ecfe57bd-82ef-3ca1-9d76-d0416bdddcb9", "abstract"=>"Long-term antibiotic use generates pan-resistant super pathogens. Anti-infective compounds that selectively disrupt virulence pathways without affecting cell viability may be used to efficiently combat infections caused by these pathogens. A candidate target pathway is quorum sensing (QS), which many bacterial pathogens use to coordinately regulate virulence determinants. The Pseudomonas aeruginosa MvfR-dependent QS regulatory pathway controls the expression of key virulence genes; and is activated via the extracellular signals 4-hydroxy-2-heptylquinoline (HHQ) and 3,4-dihydroxy-2-heptylquinoline (PQS), whose syntheses depend on anthranilic acid (AA), the primary precursor of 4-hydroxy-2-alkylquinolines (HAQs). Here, we identified halogenated AA analogs that specifically inhibited HAQ biosynthesis and disrupted MvfR-dependent gene expression. These compounds restricted P. aeruginosa systemic dissemination and mortality in mice, without perturbing bacterial viability, and inhibited osmoprotection, a widespread bacterial function. These compounds provide a starting point for the design and development of selective anti-infectives that restrict human P. aeruginosa pathogenesis, and possibly other clinically significant pathogens.", "link"=>"http://www.mendeley.com/research/inhibitors-pathogen-intercellular-signals-selective-antiinfective-compounds", "reader_count"=>102, "reader_count_by_academic_status"=>{"Unspecified"=>5, "Professor > Associate Professor"=>5, "Researcher"=>27, "Student > Doctoral Student"=>5, "Student > Ph. D. Student"=>23, "Student > Postgraduate"=>6, "Student > Master"=>10, "Other"=>2, "Student > Bachelor"=>10, "Lecturer"=>2, "Professor"=>7}, "reader_count_by_user_role"=>{"Unspecified"=>5, "Professor > Associate Professor"=>5, "Researcher"=>27, "Student > Doctoral Student"=>5, "Student > Ph. D. Student"=>23, "Student > Postgraduate"=>6, "Student > Master"=>10, "Other"=>2, "Student > Bachelor"=>10, "Lecturer"=>2, "Professor"=>7}, "reader_count_by_subject_area"=>{"Engineering"=>2, "Unspecified"=>8, "Environmental Science"=>2, "Biochemistry, Genetics and Molecular Biology"=>8, "Agricultural and Biological Sciences"=>57, "Medicine and Dentistry"=>11, "Design"=>1, "Neuroscience"=>1, "Pharmacology, Toxicology and Pharmaceutical Science"=>1, "Chemistry"=>5, "Immunology and Microbiology"=>5, "Earth and Planetary Sciences"=>1}, "reader_count_by_subdiscipline"=>{"Design"=>{"Design"=>1}, "Engineering"=>{"Engineering"=>2}, "Medicine and Dentistry"=>{"Medicine and Dentistry"=>11}, "Neuroscience"=>{"Neuroscience"=>1}, "Chemistry"=>{"Chemistry"=>5}, "Immunology and Microbiology"=>{"Immunology and Microbiology"=>5}, "Earth and Planetary Sciences"=>{"Earth and Planetary Sciences"=>1}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>57}, "Biochemistry, Genetics and Molecular Biology"=>{"Biochemistry, Genetics and Molecular Biology"=>8}, "Unspecified"=>{"Unspecified"=>8}, "Environmental Science"=>{"Environmental Science"=>2}, "Pharmacology, Toxicology and Pharmaceutical Science"=>{"Pharmacology, Toxicology and Pharmaceutical Science"=>1}}, "reader_count_by_country"=>{"Canada"=>1, "Belgium"=>2, "United States"=>2, "United Kingdom"=>1, "France"=>3, "Chile"=>1, "Germany"=>1}, "group_count"=>3}

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Figshare

  • {"files"=>["https://ndownloader.figshare.com/files/944741"], "description"=>"<div><p>(A) The AA analogs do not perturb AA accumulation. Intracellular AA concentrations (mM) were determined for PA14 cells grown minus or plus 1.5 mM 6FABA, 6CABA, or 4CABA, and for <i>pqsA</i><sup>−</sup> mutant cells.</p><p>(B) Exogenous AA partially overcomes AA analog inhibition of HHQ synthesis in PA14 cells. Increasing concentrations of AA were added to cultures grown in 0.125 mM 6FABA, 0.75 mM 6CABA, or 0.125 mM 4CABA, which reduced HHQ production by 75% in supernatants of OD<sub>600</sub> = 4 cell cultures. The competing AA concentrations were 0, 3, 6, and 10 times that of each AA analog.</p></div>", "links"=>[], "tags"=>["analogs", "aa", "pqsa"], "article_id"=>615111, "categories"=>["Microbiology", "Biochemistry", "Infectious Diseases"], "users"=>["Biliana Lesic", "François Lépine", "Eric Déziel", "Jiangwen Zhang", "Qunhao Zhang", "Katie Padfield", "Marie-Hélène Castonguay", "Sylvain Milot", "Scott Stachel", "A. Aria Tzika", "Ronald G Tompkins", "Laurence G Rahme"], "doi"=>"https://dx.doi.org/10.1371/journal.ppat.0030126.g003", "stats"=>{"downloads"=>2, "page_views"=>0, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_AA_Analogs_Compete_with_AA_for_the_PqsA_Active_Site_/615111", "title"=>"AA Analogs Compete with AA for the PqsA Active Site", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2007-09-14 01:25:11"}
  • {"files"=>["https://ndownloader.figshare.com/files/945168"], "description"=>"<p>Ten times (10×) serial dilutions of the indicated bacterial pathogens were spotted onto high-salt tester plates containing no AA analog, 6 mM 6FABA, 6 mM 6CABA, or 1.5 mM 4CABA. Note that at these concentrations, bacterial growth on regular low-salt LB plates was unaffected.</p>", "links"=>[], "tags"=>["aa", "analogs", "osmotic", "bacterial"], "article_id"=>615534, "categories"=>["Microbiology", "Biochemistry", "Infectious Diseases"], "users"=>["Biliana Lesic", "François Lépine", "Eric Déziel", "Jiangwen Zhang", "Qunhao Zhang", "Katie Padfield", "Marie-Hélène Castonguay", "Sylvain Milot", "Scott Stachel", "A. Aria Tzika", "Ronald G Tompkins", "Laurence G Rahme"], "doi"=>"https://dx.doi.org/10.1371/journal.ppat.0030126.g007", "stats"=>{"downloads"=>0, "page_views"=>0, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_The_AA_Analogs_Increase_the_Osmotic_Sensitivity_of_Several_Bacterial_Pathogens_/615534", "title"=>"The AA Analogs Increase the Osmotic Sensitivity of Several Bacterial Pathogens", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2007-09-14 01:32:14"}
  • {"files"=>["https://ndownloader.figshare.com/files/945039"], "description"=>"<p>Mass spectrometry (MS) determination of unsaturated HAQs in OD<sub>600</sub> = 3 culture supernatants of B. thailandensis cells grown in the absence or presence of 3 mM 6FABA, 6CABA, or 4CABA. Note that while saturated HAQs, including HHQ, occur in B. thailandensis cells, their levels were below the quantification threshold.</p>", "links"=>[], "tags"=>["aa", "analogs", "inhibit", "haq"], "article_id"=>615406, "categories"=>["Microbiology", "Biochemistry", "Infectious Diseases"], "users"=>["Biliana Lesic", "François Lépine", "Eric Déziel", "Jiangwen Zhang", "Qunhao Zhang", "Katie Padfield", "Marie-Hélène Castonguay", "Sylvain Milot", "Scott Stachel", "A. Aria Tzika", "Ronald G Tompkins", "Laurence G Rahme"], "doi"=>"https://dx.doi.org/10.1371/journal.ppat.0030126.g006", "stats"=>{"downloads"=>0, "page_views"=>0, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_The_AA_Analogs_Inhibit_HAQ_Production_in_B_thailandensis_Cell_Supernatants_/615406", "title"=>"The AA Analogs Inhibit HAQ Production in B. thailandensis Cell Supernatants", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2007-09-14 01:30:06"}
  • {"files"=>["https://ndownloader.figshare.com/files/944580"], "description"=>"<div><p>(A) Chemical structures of AA, MA, and five halogenated AA analogs.</p><p>(B) The HAQ biosynthetic pathway and hypothetical steps mediated by the <i>pqsA-D</i> gene products.</p></div>", "links"=>[], "tags"=>["analogs", "haq", "biosynthetic"], "article_id"=>614955, "categories"=>["Microbiology", "Biochemistry", "Infectious Diseases"], "users"=>["Biliana Lesic", "François Lépine", "Eric Déziel", "Jiangwen Zhang", "Qunhao Zhang", "Katie Padfield", "Marie-Hélène Castonguay", "Sylvain Milot", "Scott Stachel", "A. Aria Tzika", "Ronald G Tompkins", "Laurence G Rahme"], "doi"=>"https://dx.doi.org/10.1371/journal.ppat.0030126.g001", "stats"=>{"downloads"=>0, "page_views"=>0, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Anthranilic_Acid_Analogs_and_HAQ_Biosynthetic_Pathway_/614955", "title"=>"Anthranilic Acid Analogs and HAQ Biosynthetic Pathway", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2007-09-14 01:22:35"}
  • {"files"=>["https://ndownloader.figshare.com/files/944658"], "description"=>"<p>Culture supernatants of PA14 cells grown in LB media minus or plus 1.5 mM or 6 mM 6FABA, 1.5 mM or 6 mM 6CABA, 1.5 mM 4CABA, or 1.5 mM MA, were collected at 5, 10, 15, and 24 h; and HHQ, PQS, and HQNO concentrations (mg/l) were quantified by LC/MS. Data points are the average of triplicate experiments, ± standard deviation. To facilitate presentation, below-detection levels of HAQs are indicated as 0.01.</p>", "links"=>[], "tags"=>["aa", "analogs", "inhibit", "haq"], "article_id"=>615033, "categories"=>["Microbiology", "Biochemistry", "Infectious Diseases"], "users"=>["Biliana Lesic", "François Lépine", "Eric Déziel", "Jiangwen Zhang", "Qunhao Zhang", "Katie Padfield", "Marie-Hélène Castonguay", "Sylvain Milot", "Scott Stachel", "A. Aria Tzika", "Ronald G Tompkins", "Laurence G Rahme"], "doi"=>"https://dx.doi.org/10.1371/journal.ppat.0030126.g002", "stats"=>{"downloads"=>0, "page_views"=>0, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Halogenated_AA_Analogs_Inhibit_HAQ_Biosynthesis_/615033", "title"=>"Halogenated AA Analogs Inhibit HAQ Biosynthesis", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2007-09-14 01:23:53"}
  • {"files"=>["https://ndownloader.figshare.com/files/944940"], "description"=>"<p>PA14-infected mice were left untreated (controls) or injected 6 h post-B+I with 6FABA, 6CABA, or 4CABA. The animals were subsequently sacrificed at 22 h post-B+I, and bacteria CFU/mg were determined for (A) muscle tissue that directly underlies the infection site; (B) muscle tissue adjacent to the infection site; and (C) blood. Numbers above dots correspond to the number of mice for each condition. The statistical significance of the CFU/mg differences between the treated and untreated control mice were determined using a Wilcoxon rank sum test. <i>p</i>-Values for the difference in adjacent muscle in response to 6FABA, 6CABA, and 4CABA treatment versus no treatment were 0.00001, 0.00066, and 0.00267, respectively; <i>p</i>-values for the difference in blood with 6FABA, 6CABA, and 4CABA, treatment versus no treatment were 0.00147, 0.00331, and 0.00331, respectively.</p>", "links"=>[], "tags"=>["aa", "analogs", "systemic", "bacterial", "proliferation"], "article_id"=>615306, "categories"=>["Microbiology", "Biochemistry", "Infectious Diseases"], "users"=>["Biliana Lesic", "François Lépine", "Eric Déziel", "Jiangwen Zhang", "Qunhao Zhang", "Katie Padfield", "Marie-Hélène Castonguay", "Sylvain Milot", "Scott Stachel", "A. Aria Tzika", "Ronald G Tompkins", "Laurence G Rahme"], "doi"=>"https://dx.doi.org/10.1371/journal.ppat.0030126.g005", "stats"=>{"downloads"=>0, "page_views"=>0, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_The_AA_Analogs_Restrict_Systemic_Bacterial_Proliferation_but_Not_Local_Proliferation_at_the_Infection_Site_/615306", "title"=>"The AA Analogs Restrict Systemic Bacterial Proliferation, but Not Local Proliferation at the Infection Site", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2007-09-14 01:28:26"}
  • {"files"=>["https://ndownloader.figshare.com/files/465912", "https://ndownloader.figshare.com/files/465956", "https://ndownloader.figshare.com/files/466011", "https://ndownloader.figshare.com/files/466039", "https://ndownloader.figshare.com/files/466091", "https://ndownloader.figshare.com/files/466203", "https://ndownloader.figshare.com/files/466315"], "description"=>"<div><p>Long-term antibiotic use generates pan-resistant super pathogens. Anti-infective compounds that selectively disrupt virulence pathways without affecting cell viability may be used to efficiently combat infections caused by these pathogens. A candidate target pathway is quorum sensing (QS), which many bacterial pathogens use to coordinately regulate virulence determinants. The Pseudomonas aeruginosa MvfR-dependent QS regulatory pathway controls the expression of key virulence genes; and is activated via the extracellular signals 4-hydroxy-2-heptylquinoline (HHQ) and 3,4-dihydroxy-2-heptylquinoline (PQS), whose syntheses depend on anthranilic acid (AA), the primary precursor of 4-hydroxy-2-alkylquinolines (HAQs). Here, we identified halogenated AA analogs that specifically inhibited HAQ biosynthesis and disrupted MvfR-dependent gene expression. These compounds restricted P. aeruginosa systemic dissemination and mortality in mice, without perturbing bacterial viability, and inhibited osmoprotection, a widespread bacterial function. These compounds provide a starting point for the design and development of selective anti-infectives that restrict human P. aeruginosa pathogenesis, and possibly other clinically significant pathogens.</p></div>", "links"=>[], "tags"=>["inhibitors", "pathogen", "intercellular", "signals", "selective", "anti-infective", "compounds"], "article_id"=>151841, "categories"=>["Cancer", "Biochemistry", "Microbiology"], "users"=>["Biliana Lesic", "François Lépine", "Eric Déziel", "Jiangwen Zhang", "Qunhao Zhang", "Katie Padfield", "Marie-Hélène Castonguay", "Sylvain Milot", "Scott Stachel", "A. Aria Tzika", "Ronald G Tompkins", "Laurence G Rahme"], "doi"=>["https://dx.doi.org/10.1371/journal.ppat.0030126.sg001", "https://dx.doi.org/10.1371/journal.ppat.0030126.sg002", "https://dx.doi.org/10.1371/journal.ppat.0030126.sg003", "https://dx.doi.org/10.1371/journal.ppat.0030126.sg004", "https://dx.doi.org/10.1371/journal.ppat.0030126.st001", "https://dx.doi.org/10.1371/journal.ppat.0030126.st002", "https://dx.doi.org/10.1371/journal.ppat.0030126.st003"], "stats"=>{"downloads"=>70, "page_views"=>39, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/Inhibitors_of_Pathogen_Intercellular_Signals_as_Selective_Anti_Infective_Compounds/151841", "title"=>"Inhibitors of Pathogen Intercellular Signals as Selective Anti-Infective Compounds", "pos_in_sequence"=>0, "defined_type"=>4, "published_date"=>"2007-09-14 00:30:41"}
  • {"files"=>["https://ndownloader.figshare.com/files/944824"], "description"=>"<div><p>(A) PA14-infected mice were injected 6 h post-B+I with 6FABA, 6CABA, or 4CABA. Mice infected with <i>pqsA<sup>−</sup></i> cells served as an additional control group. Data were averaged for a minimum of two independent experiments, with <i>n</i>(PA14) = 40; <i>n</i>(PA14/6FABA) = 36; <i>n</i>(PA14/6CABA) = 30; <i>n</i>(PA14/4CABA) = 20 and <i>n</i>(<i>pqsA<sup>−</sup></i>) = 20. Standard deviations were <20% for the time points between 0 and 4 d, and <12% thereafter. Cox proportional hazards regression showed that mouse mortality due to PA14 infection was significantly reduced by injection with 6FABA (hazard ratio = 0.398, <i>p</i> = 5.6e-04), 6CABA (hazard ratio = 0.397, <i>p</i> = 1.2e-03), and 4CABA (hazard ratio = 0.325, <i>P</i> = 1.8e-03), compared with control saline; <i>pqsA<sup>−</sup></i> virulence was highly attenuated (hazard ratio = 0.118, <i>p</i> = 9.1e-06).</p><p>(B) HHQ levels (<i>μg</i>/mg) at 12 h post-B+I for rectus adbominus muscle directly underlying the infection site in untreated B+I mice, and for mice treated 6 h post-B+I with 6FABA, 6CABA, or 4CABA. <i>n</i> = 5 for each experimental condition. The <i>t</i>-test (<i>p</i> = 0.011) and Wilcoxon rank sum test (<i>p</i> = 0.03) showed that the difference in HHQ levels between control and 4CABA-treated mice was statistically significant.</p></div>", "links"=>[], "tags"=>["aa", "analogs", "mice", "pa14", "vivo", "hhq"], "article_id"=>615186, "categories"=>["Microbiology", "Biochemistry", "Infectious Diseases"], "users"=>["Biliana Lesic", "François Lépine", "Eric Déziel", "Jiangwen Zhang", "Qunhao Zhang", "Katie Padfield", "Marie-Hélène Castonguay", "Sylvain Milot", "Scott Stachel", "A. Aria Tzika", "Ronald G Tompkins", "Laurence G Rahme"], "doi"=>"https://dx.doi.org/10.1371/journal.ppat.0030126.g004", "stats"=>{"downloads"=>1, "page_views"=>7, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_The_AA_Analogs_Promote_Survival_of_B_I_Mice_to_PA14_Pathogenesis_and_Restrict_In_Vivo_HHQ_Production_/615186", "title"=>"The AA Analogs Promote Survival of B+I Mice to PA14 Pathogenesis, and Restrict In Vivo HHQ Production", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2007-09-14 01:26:26"}

PMC Usage Stats | Further Information

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Relative Metric

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