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Iron (Fe) in soluble elemental form is found in the tissues and fluids of animals at concentrations insufficient for sustaining growth of bacteria. Consequently, to promote colonization and persistence, pathogenic bacteria evolved a myriad of scavenging mechanisms to acquire Fe from the host.Bordetella bronchiseptica , the etiologic agent of upper respiratory infections in a wide range of mammalian hosts, expresses a number of proteins for acquisition of Fe. Using proteomic and genomic approaches, three Fe-regulated genes were identified in the bordetellae:bfrH , a gene encoding a putative siderophore receptor;ecfI , a gene encoding a putative extracellular function (ECF) sigma factor; andecfR , a gene encoding a putative EcfI modulator. All three genes are highly conserved inB. pertussis ,B. parapertussis , andB. avium . Genetic analysis revealed that transcription ofbfrH was coregulated byecfI ,ecfR , andfur1 , one of twofur homologues carried byB. bronchiseptica . Overexpression ofecfI decoupledbfrH from Fe-dependent regulation. In contrast, expression ofbfrH was significantly reduced in anecfI deletion mutant. Deletion ofecfR , however, was correlated with a significant increase in expression ofbfrH , due in part to acis -acting nucleotide sequence withinecfR which likely reduces the frequency of readthrough transcription ofbfrH from the Fe-dependentecfIR promoter. Using a murine competition infection model,bfrH was shown to be required for optimal virulence ofB. bronchiseptica . These experiments revealedecfIR -bfrH as a locus encoding a new member of the growing family of Fe and ECF sigma factor-modulated regulons in the bordetellae.

infection and immunity

Expression of BfrH, a Putative Siderophore Receptor of <i>Bordetella bronchiseptica</i> , Is Regulated by Iron, Fur1, and the Extracellular Function Sigma Factor EcfI

Expression of BfrH, a Putative Siderophore Receptor of Bordetella bronchiseptica , Is Regulated by Iron, Fur1, and the Extracellular Function Sigma Factor EcfI