title: The glutamic acid decarboxylase system of the new species Brucella microti contributes to its acid resistance and to oral infection of mice.
abstract: BACKGROUND
  Genome analysis indicated that the new species Brucella microti possesses a potentially functional glutamate decarboxylase (GAD) system involved in extreme acid resistance in several foodborne bacteria. The contribution of this system in adaptation of B. microti to an acidic environment, including the intracellular vacuole and stomach, was investigated.
  
  
  RESULTS
  B. microti was GAD positive and able to export its product, γ-aminobutyrate, to the extracellular medium. The resistance of B. microti to acid stress (pH 2.5) was glutamate dependent. Mutants affected in the GAD system lost this resistance, demonstrating its direct involvement in survival under these conditions. The reciprocal heterologous complementation of mutants with the GAD systems of Escherichia coli or B. microti confirmed conserved functions in both bacterial species. A gad mutant was not attenuated during infection of macrophages, where Brucella resides in an acidified vacuole at a pH of 4-4.5 during the early phase of macrophage infection, but GAD contributed to the survival of B. microti in a murine model following oral infection.
  
  
  CONCLUSIONS
  This work provides first evidence that the GAD system might play an essential role in the resistance of an environment-borne, pathogenic Brucella species to extreme acid shock and during passage through the host stomach following oral infection.
authors.affiliation: Université Montpellier I, Centre d’études d’agents Pathogènes et Biotechnologies pour la Santé, Montpellier, France. alessandra.occhialini@cpbs.cnrs.fr
authors.forename: Alessandra
authors.initials: A
authors.lastname: Occhialini
authors.forename: Maria Pilar
authors.initials: MP
authors.lastname: Jiménez de Bagüés
authors.forename: Bashir
authors.initials: B
authors.lastname: Saadeh
authors.forename: Daniela
authors.initials: D
authors.lastname: Bastianelli
authors.forename: Nabil
authors.initials: N
authors.lastname: Hanna
authors.forename: Daniela
authors.initials: D
authors.lastname: De Biase
authors.forename: Stephan
authors.initials: S
authors.lastname: Köhler
mesh_terms: D000143:Acids / Q000378:metabolism* / Q000633:toxicity; D000818:Animals; D002002:Brucella / Q000201:enzymology* / Q000235:genetics / Q000472:pathogenicity*; D002006:Brucellosis / Q000382:microbiology*; D004195:Disease Models, Animal; D004926:Escherichia coli / Q000201:enzymology / Q000235:genetics; D005260:Female; D017353:Gene Deletion; D005816:Genetic Complementation Test; D005968:Glutamate Decarboxylase / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D008807:Mice, Inbred BALB C; D013312:Stress, Physiological; D037521:Virulence Factors / Q000235:genetics / Q000378:metabolism*
chemical_list: D000143:Acids; D037521:Virulence Factors; D005968:Glutamate Decarboxylase