Bordetella
Timothy J. Brickman, Carin K. Vanderpool, Sandra K. Armstrong
Abstract
Timothy J. Brickman, Carin K. Vanderpool, Sandra K. Armstrong
Abstract
Bordetella pertussis, Bordetella bronchiseptica, and Bordetella parapertussis are mammalian respiratory pathogens that are highly genetically related gram-negative β-proteobacteria of the family Alcaligenaceae. This chapter summarizes the current knowledge of iron acquisition in B. pertussis, and although it is not possible to cite all of the works by investigators in the field, their research contributions have been critical to the development of this knowledge base. Bordetella toxins may alter the integrity of the epithelium, allowing serum components such as complement, and possibly lymphocytes and erythrocytes, to breach the mucosa. The Bordetella alcaligin system gene cluster spans an approximately 11-kb genomic region and includes the alcABCDER operon and the alcS and fauA genes. Transcriptional activation of Bordetella genes by AlcR is remarkably sensitive to the presence of purified deferri-alcaligin inducer. The current understanding of these systems suggests the following model for Bordetella bhu gene regulation. One study using Bordetella alcR regulator mutants failed to demonstrate an effect of alcR mutation on mouse virulence, but since alcR mutants retain some low-level capacity to produce and transport alcaligin, this result did not eliminate the possibility that alcaligin utilization contributes to Bordetella virulence. The authors postulate that the ability of Bordetella species to selectively activate the expression of the different iron systems contributes to its capacity to effectively adapt and multiply in the host environment during the course of an infection.
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Bordetella pertussis, Bordetella bronchiseptica, and Bordetella parapertussis are mammalian respiratory pathogens that are highly genetically related gram-negative β-proteobacteria of the family Alcaligenaceae. This chapter summarizes the current knowledge of iron acquisition in B. pertussis, and although it is not possible to cite all of the works by investigators in the field, their research contributions have been critical to the development of this knowledge base. Bordetella toxins may alter the integrity of the epithelium, allowing serum components such as complement, and possibly lymphocytes and erythrocytes, to breach the mucosa. The Bordetella alcaligin system gene cluster spans an approximately 11-kb genomic region and includes the alcABCDER operon and the alcS and fauA genes. Transcriptional activation of Bordetella genes by AlcR is remarkably sensitive to the presence of purified deferri-alcaligin inducer. The current understanding of these systems suggests the following model for Bordetella bhu gene regulation. One study using Bordetella alcR regulator mutants failed to demonstrate an effect of alcR mutation on mouse virulence, but since alcR mutants retain some low-level capacity to produce and transport alcaligin, this result did not eliminate the possibility that alcaligin utilization contributes to Bordetella virulence. The authors postulate that the ability of Bordetella species to selectively activate the expression of the different iron systems contributes to its capacity to effectively adapt and multiply in the host environment during the course of an infection.
Key concepts: Bordetella pertussis, Bordetella, Bordetella bronchiseptica, Microbiology, Virulence, Biology, Operon, Mutant