title: Quorum Regulated Resistance of Vibrio cholerae against Environmental Bacteriophages.
abstract: Predation by bacteriophages can significantly influence the population structure of bacterial communities. Vibrio cholerae the causative agent of cholera epidemics interacts with numerous phages in the aquatic ecosystem, and in the intestine of cholera patients. Seasonal epidemics of cholera reportedly collapse due to predation of the pathogen by phages. However, it is not clear how sufficient number of the bacteria survive to seed the environment in the subsequent epidemic season. We found that bacterial cell density-dependent gene expression termed "quorum sensing" which is regulated by signal molecules called autoinducers (AIs) can protect V. cholerae against predatory phages. V. cholerae mutant strains carrying inactivated AI synthase genes were significantly more susceptible to multiple phages compared to the parent bacteria. Likewise when mixed cultures of phage and bacteria were supplemented with exogenous autoinducers CAI-1 or AI-2 produced by recombinant strains carrying cloned AI synthase genes, increased survival of V. cholerae and a decrease in phage titer was observed. Mutational analyses suggested that the observed effects of autoinducers are mediated in part through the quorum sensing-dependent production of haemaglutinin protease, and partly through downregulation of phage receptors. These results have implication in developing strategies for phage mediated control of cholera.
authors.affiliation: Laboratory Sciences and Services Division, International Centre for Diarrhoeal Disease Research, Bangladesh, Dhaka-1212, Bangladesh.
authors.forename: M Mozammel
authors.initials: MM
authors.lastname: Hoque
authors.affiliation: Laboratory Sciences and Services Division, International Centre for Diarrhoeal Disease Research, Bangladesh, Dhaka-1212, Bangladesh.
authors.forename: Iftekhar Bin
authors.initials: IB
authors.lastname: Naser
authors.affiliation: Laboratory Sciences and Services Division, International Centre for Diarrhoeal Disease Research, Bangladesh, Dhaka-1212, Bangladesh.
authors.forename: S M Nayeemul
authors.initials: SM
authors.lastname: Bari
authors.affiliation: Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, 3610 Hamilton Walk, Philadelphia, 19104-6076 USA.
authors.forename: Jun
authors.initials: J
authors.lastname: Zhu
authors.affiliation: Department of Microbiology and Immunobiology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.
authors.forename: John J
authors.initials: JJ
authors.lastname: Mekalanos
authors.affiliation: Laboratory Sciences and Services Division, International Centre for Diarrhoeal Disease Research, Bangladesh, Dhaka-1212, Bangladesh.
authors.forename: Shah M
authors.initials: SM
authors.lastname: Faruque
mesh_terms: D000371:Agglutination; D000818:Animals; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism; D001435:Bacteriophages / Q000472:pathogenicity*; D015536:Down-Regulation; D015964:Gene Expression Regulation, Bacterial; D006714:Homoserine / Q000031:analogs & derivatives / Q000378:metabolism; D007106:Immune Sera; D007659:Ketones / Q000378:metabolism; D007783:Lactones / Q000378:metabolism; D009154:Mutation; D019081:O Antigens / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D010447:Peptide Hydrolases / Q000235:genetics / Q000378:metabolism; D053038:Quorum Sensing / Q000235:genetics / Q000502:physiology*; D011817:Rabbits; D014734:Vibrio cholerae / Q000235:genetics / Q000254:growth & development / Q000821:virology*
chemical_list: C525620:3-hydroxytridecan-4-one; D001426:Bacterial Proteins; D007106:Immune Sera; D007659:Ketones; D007783:Lactones; C091088:N-octanoylhomoserine lactone; D019081:O Antigens; D006714:Homoserine; D010447:Peptide Hydrolases