Comparative proteomic analysis of the PhoP regulon in Salmonella enterica serovar Typhi versus Typhimurium
S. Typhi, a human-restricted Salmonella enterica serovar, causes a systemic intracellular infection in humans (typhoid fever). In comparison, S. Typhimurium causes gastroenteritis in humans, but causes a systemic typhoidal illness in mice. The PhoP regulon is a well studied two component (PhoP/Q) co...
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| Published in | PloS one Vol. 4; no. 9; p. e6994 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Public Library of Science
10.09.2009
Public Library of Science (PLoS) |
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| Abstract | S. Typhi, a human-restricted Salmonella enterica serovar, causes a systemic intracellular infection in humans (typhoid fever). In comparison, S. Typhimurium causes gastroenteritis in humans, but causes a systemic typhoidal illness in mice. The PhoP regulon is a well studied two component (PhoP/Q) coordinately regulated network of genes whose expression is required for intracellular survival of S. enterica.
Using high performance liquid chromatography mass spectrometry (HPLC-MS/MS), we examined the protein expression profiles of three sequenced S. enterica strains: S. Typhimurium LT2, S. Typhi CT18, and S. Typhi Ty2 in PhoP-inducing and non-inducing conditions in vitro and compared these results to profiles of phoP(-)/Q(-) mutants derived from S. Typhimurium LT2 and S. Typhi Ty2. Our analysis identified 53 proteins in S. Typhimurium LT2 and 56 proteins in S. Typhi that were regulated in a PhoP-dependent manner. As expected, many proteins identified in S. Typhi demonstrated concordant differential expression with a homologous protein in S. Typhimurium. However, three proteins (HlyE, STY1499, and CdtB) had no homolog in S. Typhimurium. HlyE is a pore-forming toxin. STY1499 encodes a stably expressed protein of unknown function transcribed in the same operon as HlyE. CdtB is a cytolethal distending toxin associated with DNA damage, cell cycle arrest, and cellular distension. Gene expression studies confirmed up-regulation of mRNA of HlyE, STY1499, and CdtB in S. Typhi in PhoP-inducing conditions.
This study is the first protein expression study of the PhoP virulence associated regulon using strains of Salmonella mutant in PhoP, has identified three Typhi-unique proteins (CdtB, HlyE and STY1499) that are not present in the genome of the wide host-range Typhimurium, and includes the first protein expression profiling of a live attenuated bacterial vaccine studied in humans (Ty800). |
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| AbstractList | S. Typhi, a human-restricted Salmonella enterica serovar, causes a systemic intracellular infection in humans (typhoid fever). In comparison, S. Typhimurium causes gastroenteritis in humans, but causes a systemic typhoidal illness in mice. The PhoP regulon is a well studied two component (PhoP/Q) coordinately regulated network of genes whose expression is required for intracellular survival of S. enterica.
Using high performance liquid chromatography mass spectrometry (HPLC-MS/MS), we examined the protein expression profiles of three sequenced S. enterica strains: S. Typhimurium LT2, S. Typhi CT18, and S. Typhi Ty2 in PhoP-inducing and non-inducing conditions in vitro and compared these results to profiles of phoP(-)/Q(-) mutants derived from S. Typhimurium LT2 and S. Typhi Ty2. Our analysis identified 53 proteins in S. Typhimurium LT2 and 56 proteins in S. Typhi that were regulated in a PhoP-dependent manner. As expected, many proteins identified in S. Typhi demonstrated concordant differential expression with a homologous protein in S. Typhimurium. However, three proteins (HlyE, STY1499, and CdtB) had no homolog in S. Typhimurium. HlyE is a pore-forming toxin. STY1499 encodes a stably expressed protein of unknown function transcribed in the same operon as HlyE. CdtB is a cytolethal distending toxin associated with DNA damage, cell cycle arrest, and cellular distension. Gene expression studies confirmed up-regulation of mRNA of HlyE, STY1499, and CdtB in S. Typhi in PhoP-inducing conditions.
This study is the first protein expression study of the PhoP virulence associated regulon using strains of Salmonella mutant in PhoP, has identified three Typhi-unique proteins (CdtB, HlyE and STY1499) that are not present in the genome of the wide host-range Typhimurium, and includes the first protein expression profiling of a live attenuated bacterial vaccine studied in humans (Ty800). Background S. Typhi, a human-restricted Salmonella enterica serovar, causes a systemic intracellular infection in humans (typhoid fever). In comparison, S. Typhimurium causes gastroenteritis in humans, but causes a systemic typhoidal illness in mice. The PhoP regulon is a well studied two component (PhoP/Q) coordinately regulated network of genes whose expression is required for intracellular survival of S. enterica. Methodology/Principal Findings Using high performance liquid chromatography mass spectrometry (HPLC-MS/MS), we examined the protein expression profiles of three sequenced S. enterica strains: S. Typhimurium LT2, S. Typhi CT18, and S. Typhi Ty2 in PhoP-inducing and non-inducing conditions in vitro and compared these results to profiles of phoP−/Q− mutants derived from S. Typhimurium LT2 and S. Typhi Ty2. Our analysis identified 53 proteins in S. Typhimurium LT2 and 56 proteins in S. Typhi that were regulated in a PhoP-dependent manner. As expected, many proteins identified in S. Typhi demonstrated concordant differential expression with a homologous protein in S. Typhimurium. However, three proteins (HlyE, STY1499, and CdtB) had no homolog in S. Typhimurium. HlyE is a pore-forming toxin. STY1499 encodes a stably expressed protein of unknown function transcribed in the same operon as HlyE. CdtB is a cytolethal distending toxin associated with DNA damage, cell cycle arrest, and cellular distension. Gene expression studies confirmed up-regulation of mRNA of HlyE, STY1499, and CdtB in S. Typhi in PhoP-inducing conditions. Conclusions/Significance This study is the first protein expression study of the PhoP virulence associated regulon using strains of Salmonella mutant in PhoP, has identified three Typhi-unique proteins (CdtB, HlyE and STY1499) that are not present in the genome of the wide host-range Typhimurium, and includes the first protein expression profiling of a live attenuated bacterial vaccine studied in humans (Ty800). BACKGROUNDS. Typhi, a human-restricted Salmonella enterica serovar, causes a systemic intracellular infection in humans (typhoid fever). In comparison, S. Typhimurium causes gastroenteritis in humans, but causes a systemic typhoidal illness in mice. The PhoP regulon is a well studied two component (PhoP/Q) coordinately regulated network of genes whose expression is required for intracellular survival of S. enterica. METHODOLOGY/PRINCIPAL FINDINGSUsing high performance liquid chromatography mass spectrometry (HPLC-MS/MS), we examined the protein expression profiles of three sequenced S. enterica strains: S. Typhimurium LT2, S. Typhi CT18, and S. Typhi Ty2 in PhoP-inducing and non-inducing conditions in vitro and compared these results to profiles of phoP(-)/Q(-) mutants derived from S. Typhimurium LT2 and S. Typhi Ty2. Our analysis identified 53 proteins in S. Typhimurium LT2 and 56 proteins in S. Typhi that were regulated in a PhoP-dependent manner. As expected, many proteins identified in S. Typhi demonstrated concordant differential expression with a homologous protein in S. Typhimurium. However, three proteins (HlyE, STY1499, and CdtB) had no homolog in S. Typhimurium. HlyE is a pore-forming toxin. STY1499 encodes a stably expressed protein of unknown function transcribed in the same operon as HlyE. CdtB is a cytolethal distending toxin associated with DNA damage, cell cycle arrest, and cellular distension. Gene expression studies confirmed up-regulation of mRNA of HlyE, STY1499, and CdtB in S. Typhi in PhoP-inducing conditions. CONCLUSIONS/SIGNIFICANCEThis study is the first protein expression study of the PhoP virulence associated regulon using strains of Salmonella mutant in PhoP, has identified three Typhi-unique proteins (CdtB, HlyE and STY1499) that are not present in the genome of the wide host-range Typhimurium, and includes the first protein expression profiling of a live attenuated bacterial vaccine studied in humans (Ty800). Background S. Typhi, a human-restricted Salmonella enterica serovar, causes a systemic intracellular infection in humans (typhoid fever). In comparison, S. Typhimurium causes gastroenteritis in humans, but causes a systemic typhoidal illness in mice. The PhoP regulon is a well studied two component (PhoP/Q) coordinately regulated network of genes whose expression is required for intracellular survival of S. enterica. Methodology/Principal Findings Using high performance liquid chromatography mass spectrometry (HPLC-MS/MS), we examined the protein expression profiles of three sequenced S. enterica strains: S. Typhimurium LT2, S. Typhi CT18, and S. Typhi Ty2 in PhoP-inducing and non-inducing conditions in vitro and compared these results to profiles of phoP−/Q− mutants derived from S. Typhimurium LT2 and S. Typhi Ty2. Our analysis identified 53 proteins in S. Typhimurium LT2 and 56 proteins in S. Typhi that were regulated in a PhoP-dependent manner. As expected, many proteins identified in S. Typhi demonstrated concordant differential expression with a homologous protein in S. Typhimurium. However, three proteins (HlyE, STY1499, and CdtB) had no homolog in S. Typhimurium. HlyE is a pore-forming toxin. STY1499 encodes a stably expressed protein of unknown function transcribed in the same operon as HlyE. CdtB is a cytolethal distending toxin associated with DNA damage, cell cycle arrest, and cellular distension. Gene expression studies confirmed up-regulation of mRNA of HlyE, STY1499, and CdtB in S. Typhi in PhoP-inducing conditions. Conclusions/Significance This study is the first protein expression study of the PhoP virulence associated regulon using strains of Salmonella mutant in PhoP, has identified three Typhi-unique proteins (CdtB, HlyE and STY1499) that are not present in the genome of the wide host-range Typhimurium, and includes the first protein expression profiling of a live attenuated bacterial vaccine studied in humans (Ty800). S. Typhi, a human-restricted Salmonella enterica serovar, causes a systemic intracellular infection in humans (typhoid fever). In comparison, S. Typhimurium causes gastroenteritis in humans, but causes a systemic typhoidal illness in mice. The PhoP regulon is a well studied two component (PhoP/Q) coordinately regulated network of genes whose expression is required for intracellular survival of S. enterica. Using high performance liquid chromatography mass spectrometry (HPLC-MS/MS), we examined the protein expression profiles of three sequenced S. enterica strains: S. Typhimurium LT2, S. Typhi CT18, and S. Typhi Ty2 in PhoP-inducing and non-inducing conditions in vitro and compared these results to profiles of phoP.sup.- /Q.sup.- mutants derived from S. Typhimurium LT2 and S. Typhi Ty2. Our analysis identified 53 proteins in S. Typhimurium LT2 and 56 proteins in S. Typhi that were regulated in a PhoP-dependent manner. As expected, many proteins identified in S. Typhi demonstrated concordant differential expression with a homologous protein in S. Typhimurium. However, three proteins (HlyE, STY1499, and CdtB) had no homolog in S. Typhimurium. HlyE is a pore-forming toxin. STY1499 encodes a stably expressed protein of unknown function transcribed in the same operon as HlyE. CdtB is a cytolethal distending toxin associated with DNA damage, cell cycle arrest, and cellular distension. Gene expression studies confirmed up-regulation of mRNA of HlyE, STY1499, and CdtB in S. Typhi in PhoP-inducing conditions. This study is the first protein expression study of the PhoP virulence associated regulon using strains of Salmonella mutant in PhoP, has identified three Typhi-unique proteins (CdtB, HlyE and STY1499) that are not present in the genome of the wide host-range Typhimurium, and includes the first protein expression profiling of a live attenuated bacterial vaccine studied in humans (Ty800). Background S. Typhi, a human-restricted Salmonella enterica serovar, causes a systemic intracellular infection in humans (typhoid fever). In comparison, S. Typhimurium causes gastroenteritis in humans, but causes a systemic typhoidal illness in mice. The PhoP regulon is a well studied two component (PhoP/Q) coordinately regulated network of genes whose expression is required for intracellular survival of S. enterica. Methodology/Principal Findings Using high performance liquid chromatography mass spectrometry (HPLC-MS/MS), we examined the protein expression profiles of three sequenced S. enterica strains: S. Typhimurium LT2, S. Typhi CT18, and S. Typhi Ty2 in PhoP-inducing and non-inducing conditions in vitro and compared these results to profiles of phoP.sup.- /Q.sup.- mutants derived from S. Typhimurium LT2 and S. Typhi Ty2. Our analysis identified 53 proteins in S. Typhimurium LT2 and 56 proteins in S. Typhi that were regulated in a PhoP-dependent manner. As expected, many proteins identified in S. Typhi demonstrated concordant differential expression with a homologous protein in S. Typhimurium. However, three proteins (HlyE, STY1499, and CdtB) had no homolog in S. Typhimurium. HlyE is a pore-forming toxin. STY1499 encodes a stably expressed protein of unknown function transcribed in the same operon as HlyE. CdtB is a cytolethal distending toxin associated with DNA damage, cell cycle arrest, and cellular distension. Gene expression studies confirmed up-regulation of mRNA of HlyE, STY1499, and CdtB in S. Typhi in PhoP-inducing conditions. Conclusions/Significance This study is the first protein expression study of the PhoP virulence associated regulon using strains of Salmonella mutant in PhoP, has identified three Typhi-unique proteins (CdtB, HlyE and STY1499) that are not present in the genome of the wide host-range Typhimurium, and includes the first protein expression profiling of a live attenuated bacterial vaccine studied in humans (Ty800). BACKGROUND:S. Typhi, a human-restricted Salmonella enterica serovar, causes a systemic intracellular infection in humans (typhoid fever). In comparison, S. Typhimurium causes gastroenteritis in humans, but causes a systemic typhoidal illness in mice. The PhoP regulon is a well studied two component (PhoP/Q) coordinately regulated network of genes whose expression is required for intracellular survival of S. enterica. METHODOLOGY/PRINCIPAL FINDINGS:Using high performance liquid chromatography mass spectrometry (HPLC-MS/MS), we examined the protein expression profiles of three sequenced S. enterica strains: S. Typhimurium LT2, S. Typhi CT18, and S. Typhi Ty2 in PhoP-inducing and non-inducing conditions in vitro and compared these results to profiles of phoP(-)/Q(-) mutants derived from S. Typhimurium LT2 and S. Typhi Ty2. Our analysis identified 53 proteins in S. Typhimurium LT2 and 56 proteins in S. Typhi that were regulated in a PhoP-dependent manner. As expected, many proteins identified in S. Typhi demonstrated concordant differential expression with a homologous protein in S. Typhimurium. However, three proteins (HlyE, STY1499, and CdtB) had no homolog in S. Typhimurium. HlyE is a pore-forming toxin. STY1499 encodes a stably expressed protein of unknown function transcribed in the same operon as HlyE. CdtB is a cytolethal distending toxin associated with DNA damage, cell cycle arrest, and cellular distension. Gene expression studies confirmed up-regulation of mRNA of HlyE, STY1499, and CdtB in S. Typhi in PhoP-inducing conditions. CONCLUSIONS/SIGNIFICANCE:This study is the first protein expression study of the PhoP virulence associated regulon using strains of Salmonella mutant in PhoP, has identified three Typhi-unique proteins (CdtB, HlyE and STY1499) that are not present in the genome of the wide host-range Typhimurium, and includes the first protein expression profiling of a live attenuated bacterial vaccine studied in humans (Ty800). |
| Audience | Academic |
| Author | LaRocque, Regina C Ryan, Edward T Calderwood, Stephen B Harris, Jason B Sheikh, Alaullah Lebrun, Lauren M Qadri, Firdausi Rollins, Sean M Hohmann, Elizabeth L Sarracino, David A Logvinenko, Tanya Rosenberg, Ian Chase, Michael R Charles, Richelle C Krastins, Bryan Tarique, Abdullah |
| AuthorAffiliation | 4 Harvard Medical School–Partners Healthcare Center for Genetics and Genomics, Cambridge, Massachusetts, United States of America 8 Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts, United States of America 3 Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, United States of America University of Hyderabad, India 2 Department of Medicine, Harvard Medical School, Boston, Massachusetts, United States of America 7 Biostatistics Research Center, Tufts Medical Center, Boston, Massachusetts, United States of America 1 Division of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts, United States of America 5 Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts, United States of America 6 International Centre for Diarrhoeal Disease Research, Bangladesh, Dhaka, Bangladesh |
| AuthorAffiliation_xml | – name: 5 Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts, United States of America – name: 1 Division of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts, United States of America – name: 3 Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, United States of America – name: 6 International Centre for Diarrhoeal Disease Research, Bangladesh, Dhaka, Bangladesh – name: 4 Harvard Medical School–Partners Healthcare Center for Genetics and Genomics, Cambridge, Massachusetts, United States of America – name: 2 Department of Medicine, Harvard Medical School, Boston, Massachusetts, United States of America – name: 7 Biostatistics Research Center, Tufts Medical Center, Boston, Massachusetts, United States of America – name: 8 Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts, United States of America – name: University of Hyderabad, India |
| Author_xml | – sequence: 1 givenname: Richelle C surname: Charles fullname: Charles, Richelle C email: rccharles@partners.org organization: Division of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts, USA. rccharles@partners.org – sequence: 2 givenname: Jason B surname: Harris fullname: Harris, Jason B – sequence: 3 givenname: Michael R surname: Chase fullname: Chase, Michael R – sequence: 4 givenname: Lauren M surname: Lebrun fullname: Lebrun, Lauren M – sequence: 5 givenname: Alaullah surname: Sheikh fullname: Sheikh, Alaullah – sequence: 6 givenname: Regina C surname: LaRocque fullname: LaRocque, Regina C – sequence: 7 givenname: Tanya surname: Logvinenko fullname: Logvinenko, Tanya – sequence: 8 givenname: Sean M surname: Rollins fullname: Rollins, Sean M – sequence: 9 givenname: Abdullah surname: Tarique fullname: Tarique, Abdullah – sequence: 10 givenname: Elizabeth L surname: Hohmann fullname: Hohmann, Elizabeth L – sequence: 11 givenname: Ian surname: Rosenberg fullname: Rosenberg, Ian – sequence: 12 givenname: Bryan surname: Krastins fullname: Krastins, Bryan – sequence: 13 givenname: David A surname: Sarracino fullname: Sarracino, David A – sequence: 14 givenname: Firdausi surname: Qadri fullname: Qadri, Firdausi – sequence: 15 givenname: Stephen B surname: Calderwood fullname: Calderwood, Stephen B – sequence: 16 givenname: Edward T surname: Ryan fullname: Ryan, Edward T |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/19746165$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | COPYRIGHT 2009 Public Library of Science 2009 Charles et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. Charles et al. 2009 |
| Copyright_xml | – notice: COPYRIGHT 2009 Public Library of Science – notice: 2009 Charles et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. – notice: Charles et al. 2009 |
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| DOI | 10.1371/journal.pone.0006994 |
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| Editor | Ahmed, Niyaz |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Conceived and designed the experiments: RCC JBH AS RCL ELH FQ SBC ETR. Performed the experiments: RCC JBH MRC LML AS SMR AT IR BK DAS. Analyzed the data: RCC JBH MRC LML AS RCL TL AT IR BK DAS SBC ETR. Contributed reagents/materials/analysis tools: MRC ELH IR BK DAS. Wrote the paper: RCC JBH MRC LML AS TL AT ELH IR BK DAS FQ SBC ETR. |
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| References | O Carmel-Harel (ref46) 2000; 54 L Shi (ref22) 2006; 281 S Lejona (ref10) 2003; 185 B Zhang (ref34) 2006; 5 J Oscarsson (ref53) 2002; 70 A Kato (ref11) 2008; 631 XH Lai (ref56) 2000; 68 X Tu (ref19) 2006; 103 F Daigle (ref26) 2001; 41 MM Wosten (ref45) 1999; 274 JA Crump (ref1) 2004; 82 FC Soncini (ref12) 1996; 178 J Parkhill (ref3) 2001; 413 S Spano (ref49) 2008; 3 I Hautefort (ref27) 2008; 10 M Westermark (ref54) 2000; 182 FC Soncini (ref39) 1995; 177 PI Fields (ref6) 1989; 243 A Kato (ref40) 1999; 181 NR Wyborn (ref55) 2004; 186 WJ Belden (ref37) 1994; 62 EA Groisman (ref15) 2006; 4 SP Faucher (ref38) 2009; 155 K Yamamoto (ref41) 2002; 45 SI Miller (ref30) 1989; 86 E Haghjoo (ref50) 2007; 64 LD Kier (ref32) 1979; 138 C Mouslim (ref44) 2003; 47 SP Faucher (ref24) 2005; 73 E Haghjoo (ref48) 2004; 101 A Spory (ref42) 2002; 184 WW Navarre (ref60) 2005; 56 SJ Libby (ref51) 1994; 91 E Garcia Vescovi (ref13) 1994; 145 I Behlau (ref31) 1993; 175 JK Lithgow (ref52) 2007; 66 VA Norte (ref18) 2003; 185 SP Faucher (ref25) 2006; 103 EL Hohmann (ref28) 1996; 173 E Garcia Vescovi (ref14) 1996; 84 JJ Bijlsma (ref16) 2005; 57 JE Elias (ref33) 2007; 4 C Ansong (ref20) 2008; 7 C von Rhein (ref57) 2006; 74 JN Adkins (ref21) 2006; 5 N Buchmeier (ref58) 1997; 65 CM Parry (ref2) 2002; 347 C von Rhein (ref59) 2008 P Monsieurs (ref9) 2005; 60 S Eriksson (ref23) 2003; 47 PI Fields (ref7) 1986; 83 LF Kox (ref17) 2000; 19 SI Miller (ref5) 1993; 11 BJ Haas (ref35) 2004; 20 A Aguirre (ref43) 2000; 182 E Bjur (ref47) 2006; 74 I Zwir (ref8) 2005; 102 CN Kotton (ref29) 2006; 24 RC Larocque (ref36) 2005; 73 EA Groisman (ref4) 2001; 183 |
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| Snippet | S. Typhi, a human-restricted Salmonella enterica serovar, causes a systemic intracellular infection in humans (typhoid fever). In comparison, S. Typhimurium... Background S. Typhi, a human-restricted Salmonella enterica serovar, causes a systemic intracellular infection in humans (typhoid fever). In comparison, S.... BACKGROUNDS. Typhi, a human-restricted Salmonella enterica serovar, causes a systemic intracellular infection in humans (typhoid fever). In comparison, S.... BACKGROUND:S. Typhi, a human-restricted Salmonella enterica serovar, causes a systemic intracellular infection in humans (typhoid fever). In comparison, S.... Background S. Typhi, a human-restricted Salmonella enterica serovar, causes a systemic intracellular infection in humans (typhoid fever). In comparison, S.... |
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| SubjectTerms | Animals Bacteria Bacterial Proteins - metabolism Bacterial Vaccines - metabolism Cell cycle Chromatography Chromosomes Comparative analysis Cytolethal distending toxin Deoxyribonucleic acid Distension DNA DNA damage E coli Escherichia coli Fever Gastroenteritis Gene expression Gene Expression Regulation, Bacterial Genetics and Genomics/Gene Expression Genomes Genomics Health aspects High performance liquid chromatography Homology Hospitals Humans Illnesses Immunology Infectious Diseases Infectious Diseases/Bacterial Infections Infectious Diseases/Gastrointestinal Infections Infectious Diseases/Neglected Tropical Diseases Intracellular Liquid chromatography Mass spectrometry Mass spectroscopy Medical research Medical schools Medicine Mice Microbiology Microbiology/Cellular Microbiology and Pathogenesis Microbiology/Immunity to Infections Models, Biological Mutants Mutation Oxidative stress Peptides Peptides - chemistry Pore formation Proteins Proteomics - methods Public health Regulation RNA Salmonella Salmonella food poisoning Salmonella typhi - metabolism Salmonella Typhimurium Salmonella typhimurium - metabolism Species Specificity Strains (organisms) Typhoid Typhoid fever Virulence Virulence (Microbiology) Virulence - genetics Water-borne diseases Waterborne diseases |
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| Title | Comparative proteomic analysis of the PhoP regulon in Salmonella enterica serovar Typhi versus Typhimurium |
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