Environmental sensing mechanisms in Bordetella
- PMID: 11407112
- DOI: 10.1016/s0065-2911(01)44013-6
Environmental sensing mechanisms in Bordetella
Abstract
The success of a bacterial pathogen may depend on its ability to sense and respond to different environments. This is particularly true of those pathogens whose survival depends on adaptation to different niches both within and outside the host. Members of the genus Bordetella cause infections in humans, other animals and birds. Two closely related species, B. pertussis and B. bronchiseptica, cause respiratory disease and express a similar range of virulence factors during infection, but exhibit different host ranges and responses to environmental change. B. pertussis has no known reservoir other than humans and is assumed to be transmitted directly via aerosol droplets between hosts. B. bronchiseptica, on the other hand, has the potential to survive and grow in the natural environment. Comparison of the manner in which these two organisms respond to external signals has provided important insights into the co-ordinate regulation of gene expression as a response to a changing environment. During infection, both species produce a range of virulence factors whose expression is co-ordinated by two members of the two-component family of signal transduction proteins, the bvg (bordetella virulence gene) and ris (regulator of intracellular stress response) loci. When active, the bvg locus directs the activity of a number of virulence determinants in both species whose products, such as adhesins and toxins, establish colonization of the host by the bacteria, although each organism has evolved a slightly different strategy during pathogenesis. B. pertussis, the causative agent of whooping cough, promotes an acute disease and tends to be more virulent than B. bronchiseptica which generally causes chronic and persistent asymptomatic colonization of the respiratory tract. The recently identified ris locus appears to control the expression of factors important for intracellular survival of B. bronchiseptica, but a role for this regulatory locus in B. pertussis infection has not been established. Expression of the virulence determinants controlled by the bvg and ris loci is subject to modulation by different environmental signals, such as low temperature, which act through these two-component systems. Evidence indicates that, for B. bronchiseptica, bvg-controlled determinants expressed under modulating conditions, such as motility, facilitate adaptation and survival in environments outside the host. With B. pertussis, however, there is no apparent requirement for prolonged survival outside the host and this difference is reflected in the expression of different, as yet uncharacterized, determinants as a response to modulating signals. The nature of the gene products involved and their assumed role in the life cycle of B. pertussis remains to be determined. Thus, comparative analysis of these species provides an excellent model for understanding the genetic requirements for pathogenesis of respiratory infection and adaptation to changing environments, both within and outside the host.
Similar articles
-
Comparative analysis of the virulence control systems of Bordetella pertussis and Bordetella bronchiseptica.Mol Microbiol. 1996 Dec;22(5):895-908. doi: 10.1046/j.1365-2958.1996.01538.x. Mol Microbiol. 1996. PMID: 8971711
-
Neither the Bvg- phase nor the vrg6 locus of Bordetella pertussis is required for respiratory infection in mice.Infect Immun. 1998 Jun;66(6):2762-8. doi: 10.1128/IAI.66.6.2762-2768.1998. Infect Immun. 1998. PMID: 9596745 Free PMC article.
-
Nuanced differences in adenylate cyclase toxin production, acylation, and secretion may contribute to the evolution of virulence in Bordetella species.mBio. 2025 Jun 11;16(6):e0108225. doi: 10.1128/mbio.01082-25. Epub 2025 May 19. mBio. 2025. PMID: 40387377 Free PMC article.
-
The BvgAS two-component system of Bordetella spp.: a versatile modulator of virulence gene expression.Int J Med Microbiol. 2001 May;291(2):119-30. doi: 10.1078/1438-4221-00109. Int J Med Microbiol. 2001. PMID: 11437335 Review.
-
Mechanisms of Bordetella pathogenesis.Front Biosci. 2001 Nov 1;6:E168-86. doi: 10.2741/mattoo. Front Biosci. 2001. PMID: 11689354 Review.
Cited by
-
Bordetella bronchiseptica exploits the complex life cycle of Dictyostelium discoideum as an amplifying transmission vector.PLoS Biol. 2017 Apr 12;15(4):e2000420. doi: 10.1371/journal.pbio.2000420. eCollection 2017 Apr. PLoS Biol. 2017. PMID: 28403138 Free PMC article.
-
Characterization of the mrgRS locus of the opportunistic pathogen Burkholderia pseudomallei: temperature regulates the expression of a two-component signal transduction system.BMC Microbiol. 2006 Aug 7;6:70. doi: 10.1186/1471-2180-6-70. BMC Microbiol. 2006. PMID: 16893462 Free PMC article.
-
Evolution of Bordetellae from Environmental Microbes to Human Respiratory Pathogens: Amoebae as a Missing Link.Front Cell Infect Microbiol. 2017 Dec 11;7:510. doi: 10.3389/fcimb.2017.00510. eCollection 2017. Front Cell Infect Microbiol. 2017. PMID: 29322035 Free PMC article.
-
The putative response regulator BaeR stimulates multidrug resistance of Escherichia coli via a novel multidrug exporter system, MdtABC.J Bacteriol. 2002 Aug;184(15):4161-7. doi: 10.1128/JB.184.15.4161-4167.2002. J Bacteriol. 2002. PMID: 12107133 Free PMC article.
-
Alcaligin siderophore production by Bordetella bronchiseptica strain RB50 is not repressed by the BvgAS virulence control system.J Bacteriol. 2002 Dec;184(24):7055-7. doi: 10.1128/JB.184.24.7055-7057.2002. J Bacteriol. 2002. PMID: 12446655 Free PMC article.