title: Spermine and Spermidine Alter Gene Expression and Antigenic Profile of Borrelia burgdorferi.
abstract: Borrelia burgdorferi, the agent of Lyme disease, responds to numerous host-derived signals to alter adaptive capabilities during its enzootic cycle in an arthropod vector and mammalian host. Molecular mechanisms that enableB. burgdorferito detect, channel, and respond to these signals have become an intense area of study for developing strategies to limit transmission/infection. Bioinformatic analysis of the borrelial genome revealed the presence of polyamine transport components (PotA, PotB, PotC, and PotD), while homologs for polyamine biosynthesis were conspicuously absent. AlthoughpotABCDis cotranscribed, the level of PotA was elevated underin vitrogrowth conditions mimicking unfed ticks compared to the level in fed ticks, while the levels of PotD were similar under the aforementioned conditions inB. burgdorferiAmong several polyamines and polyamine precursors, supplementation of spermine or spermidine in the borrelial growth medium induced synthesis of major regulators of gene expression inB. burgdorferi, such as RpoS and BosR, with a concomitant increase in proteins that contribute to colonization and survival ofB. burgdorferiin the mammalian host. Short transcripts ofrpoSwere elevated in response to spermidine, which was correlated with increased protein levels of RpoS. Transcriptional analysis ofrpoZandB. burgdorferirel(relBbu;bb0198) in the presence of spermidine revealed the interplay of multiple regulatory factors inB. burgdorferigene expression. The effect of spermidine on the levels of select borrelial proteins was also influenced by serum factors. These studies suggest that multiple host-derived signals/nutrients and their transport systems contribute toB. burgdorferiadaptation during the vector and vertebrate host phases of infection.
authors.affiliation: South Texas Center for Emerging Infectious Diseases, Center of Excellence in Infection Genomics and Department of Biology, The University of Texas at San Antonio, San Antonio, Texas, USA.
authors.forename: Ying-Han
authors.initials: YH
authors.lastname: Lin
authors.affiliation: South Texas Center for Emerging Infectious Diseases, Center of Excellence in Infection Genomics and Department of Biology, The University of Texas at San Antonio, San Antonio, Texas, USA.
authors.forename: Jesus A
authors.initials: JA
authors.lastname: Romo
authors.affiliation: South Texas Center for Emerging Infectious Diseases, Center of Excellence in Infection Genomics and Department of Biology, The University of Texas at San Antonio, San Antonio, Texas, USA.
authors.forename: Trever C
authors.initials: TC
authors.lastname: Smith
authors.affiliation: South Texas Center for Emerging Infectious Diseases, Center of Excellence in Infection Genomics and Department of Biology, The University of Texas at San Antonio, San Antonio, Texas, USA.
authors.forename: Ann N
authors.initials: AN
authors.lastname: Reyes
authors.affiliation: South Texas Center for Emerging Infectious Diseases, Center of Excellence in Infection Genomics and Department of Biology, The University of Texas at San Antonio, San Antonio, Texas, USA.
authors.forename: S L Rajasekhar
authors.initials: SLR
authors.lastname: Karna
authors.affiliation: South Texas Center for Emerging Infectious Diseases, Center of Excellence in Infection Genomics and Department of Biology, The University of Texas at San Antonio, San Antonio, Texas, USA.
authors.forename: Christine L
authors.initials: CL
authors.lastname: Miller
authors.affiliation: Department of Biology, California State University Fresno, Fresno, California, USA.
authors.forename: Tricia A
authors.initials: TA
authors.lastname: Van Laar
authors.affiliation: Feik School of Pharmacy, University of The Incarnate Word, San Antonio, Texas, USA.
authors.forename: Raghunandan
authors.initials: R
authors.lastname: Yendapally
authors.affiliation: South Texas Center for Emerging Infectious Diseases, Center of Excellence in Infection Genomics and Department of Biology, The University of Texas at San Antonio, San Antonio, Texas, USA.
authors.forename: James P
authors.initials: JP
authors.lastname: Chambers
authors.affiliation: South Texas Center for Emerging Infectious Diseases, Center of Excellence in Infection Genomics and Department of Biology, The University of Texas at San Antonio, San Antonio, Texas, USA j.seshu@utsa.edu.
authors.forename: J
authors.initials: J
authors.lastname: Seshu
mesh_terms: D000942:Antigens, Bacterial / Q000235:genetics* / Q000276:immunology*; D001426:Bacterial Proteins / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D001692:Biological Transport; D025065:Borrelia burgdorferi / Q000502:physiology*; D015964:Gene Expression Regulation, Bacterial / Q000187:drug effects; D006801:Humans; D008193:Lyme Disease / Q000276:immunology / Q000382:microbiology; D011073:Polyamines / Q000378:metabolism / Q000494:pharmacology; D013095:Spermidine / Q000378:metabolism* / Q000494:pharmacology; D013096:Spermine / Q000378:metabolism* / Q000494:pharmacology; D014158:Transcription, Genetic; D037521:Virulence Factors / Q000235:genetics
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D011073:Polyamines; D037521:Virulence Factors; D013096:Spermine; D013095:Spermidine
keywords: Borrelia burgdorferi; Lyme disease; polyamines