Supplementary material for "Interplay Of Virulence Factors and Signaling Molecules: Albumin And Calcium-Mediated Biofilm Regulation In Bordetella bronchiseptia"

Autores
Mugni, Sabrina Laura; Ambrosis, Nicolás Martín; O'Toole, George A.; Sisti, Federico; Fernández, Julieta
Año de publicación
2025
Idioma
inglés
Tipo de recurso
conjunto de datos
Estado
versión publicada
Descripción
Bordetella bronchiseptica, a respiratory pathogen capable of infecting various mammals, including humans, is associated with chronic infections, contrasting with the acute infections caused by B. pertussis. Both pathogens can form biofilm-like structures in vivo, providing tolerance against environmental stresses. Biofilm formation in B. bronchiseptica is regulated by the BvgAS two-component system, with intermediate concentrations of certain modulators inducing a phase favoring biofilm formation. Recent studies have highlighted the role of cyclic diguanylate monophosphate (c-di-GMP) in this process: elevated c-di-GMP levels stimulate biofilm formation, whereas phosphodiesterase (PDE) activation reduces biofilms. Respiratory secretions, which contain albumin and calcium at higher concentrations than standard growth media, promote an increase in the amount and localization of the adenylate cyclase toxin (AC), an important Bordetella virulence factor. Secreted AC present in the extracellular media or attached to the outer membrane inhibits biofilm formation. Based on these observations, we hypothesized that serum albumin and calcium inhibit biofilm formation and explored the involvement of c-di-GMP in this process. Our findings demonstrate that albumin and calcium inhibit B. bronchiseptica biofilm formation by two apparently independent mechanisms, formation, increasing with AC secretion playing a significant role, while the filamentous hemagglutinin adhesin (FHA) does not appear to be directly involved. Furthermore,and inducing c-di-GMP degradation. regulates biofilm formation in response to albumin and calcium. This study enhances our understanding of the complex mechanisms governing B. bronchiseptica biofilm formation and its modulation by host factors.
Fil: Mugni, Sabrina Laura. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Argentina. Fil: Ambrosis, Nicolás Martín. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Argentina. Fil: O'Toole, George A. Geisel School of Medicine at Dartmouth, Hanover. Department of Microbiology and Immunology. Estados Unidos. Fil: Sisti, Federico. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Argentina. Fil: Fernández, Julieta. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Argentina.
Instituto de Biotecnología y Biología Molecular
Materia
Ciencias Exactas
Bordetella
Biofilm
Interplay
Nivel de accesibilidad
acceso abierto
Condiciones de uso
http://creativecommons.org/licenses/by-nc-sa/4.0/
Repositorio
SEDICI (UNLP)
Institución
Universidad Nacional de La Plata
OAI Identificador
oai:sedici.unlp.edu.ar:10915/177239

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spelling Supplementary material for "Interplay Of Virulence Factors and Signaling Molecules: Albumin And Calcium-Mediated Biofilm Regulation In Bordetella bronchiseptia"Mugni, Sabrina LauraAmbrosis, Nicolás MartínO'Toole, George A.Sisti, FedericoFernández, JulietaCiencias Exactashttps://purl.org/becyt/ford/1.6BordetellaBiofilmInterplayBordetella bronchiseptica, a respiratory pathogen capable of infecting various mammals, including humans, is associated with chronic infections, contrasting with the acute infections caused by B. pertussis. Both pathogens can form biofilm-like structures in vivo, providing tolerance against environmental stresses. Biofilm formation in B. bronchiseptica is regulated by the BvgAS two-component system, with intermediate concentrations of certain modulators inducing a phase favoring biofilm formation. Recent studies have highlighted the role of cyclic diguanylate monophosphate (c-di-GMP) in this process: elevated c-di-GMP levels stimulate biofilm formation, whereas phosphodiesterase (PDE) activation reduces biofilms. Respiratory secretions, which contain albumin and calcium at higher concentrations than standard growth media, promote an increase in the amount and localization of the adenylate cyclase toxin (AC), an important Bordetella virulence factor. Secreted AC present in the extracellular media or attached to the outer membrane inhibits biofilm formation. Based on these observations, we hypothesized that serum albumin and calcium inhibit biofilm formation and explored the involvement of c-di-GMP in this process. Our findings demonstrate that albumin and calcium inhibit B. bronchiseptica biofilm formation by two apparently independent mechanisms, formation, increasing with AC secretion playing a significant role, while the filamentous hemagglutinin adhesin (FHA) does not appear to be directly involved. Furthermore,and inducing c-di-GMP degradation. regulates biofilm formation in response to albumin and calcium. This study enhances our understanding of the complex mechanisms governing B. bronchiseptica biofilm formation and its modulation by host factors.Fil: Mugni, Sabrina Laura. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Argentina. Fil: Ambrosis, Nicolás Martín. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Argentina. Fil: O'Toole, George A. Geisel School of Medicine at Dartmouth, Hanover. Department of Microbiology and Immunology. Estados Unidos. Fil: Sisti, Federico. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Argentina. Fil: Fernández, Julieta. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Argentina.Instituto de Biotecnología y Biología Molecular2025info:eu-repo/semantics/publishedVersionConjunto de datoshttp://purl.org/coar/resource_type/c_ddb1info:ar-repo/semantics/conjuntoDeDatosinfo:eu-repo/semantics/dataSetapplication/pdfhttp://sedici.unlp.edu.ar/handle/10915/177239https://doi.org/10.35537/10915/177239enginfo:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by-nc-sa/4.0/Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-09-29T11:47:54Zoai:sedici.unlp.edu.ar:10915/177239Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-29 11:47:54.312SEDICI (UNLP) - Universidad Nacional de La Platafalse
dc.title.none.fl_str_mv Supplementary material for "Interplay Of Virulence Factors and Signaling Molecules: Albumin And Calcium-Mediated Biofilm Regulation In Bordetella bronchiseptia"
title Supplementary material for "Interplay Of Virulence Factors and Signaling Molecules: Albumin And Calcium-Mediated Biofilm Regulation In Bordetella bronchiseptia"
spellingShingle Supplementary material for "Interplay Of Virulence Factors and Signaling Molecules: Albumin And Calcium-Mediated Biofilm Regulation In Bordetella bronchiseptia"
Mugni, Sabrina Laura
Ciencias Exactas
Bordetella
Biofilm
Interplay
title_short Supplementary material for "Interplay Of Virulence Factors and Signaling Molecules: Albumin And Calcium-Mediated Biofilm Regulation In Bordetella bronchiseptia"
title_full Supplementary material for "Interplay Of Virulence Factors and Signaling Molecules: Albumin And Calcium-Mediated Biofilm Regulation In Bordetella bronchiseptia"
title_fullStr Supplementary material for "Interplay Of Virulence Factors and Signaling Molecules: Albumin And Calcium-Mediated Biofilm Regulation In Bordetella bronchiseptia"
title_full_unstemmed Supplementary material for "Interplay Of Virulence Factors and Signaling Molecules: Albumin And Calcium-Mediated Biofilm Regulation In Bordetella bronchiseptia"
title_sort Supplementary material for "Interplay Of Virulence Factors and Signaling Molecules: Albumin And Calcium-Mediated Biofilm Regulation In Bordetella bronchiseptia"
dc.creator.none.fl_str_mv Mugni, Sabrina Laura
Ambrosis, Nicolás Martín
O'Toole, George A.
Sisti, Federico
Fernández, Julieta
author Mugni, Sabrina Laura
author_facet Mugni, Sabrina Laura
Ambrosis, Nicolás Martín
O'Toole, George A.
Sisti, Federico
Fernández, Julieta
author_role author
author2 Ambrosis, Nicolás Martín
O'Toole, George A.
Sisti, Federico
Fernández, Julieta
author2_role author
author
author
author
dc.subject.none.fl_str_mv Ciencias Exactas
Bordetella
Biofilm
Interplay
topic Ciencias Exactas
Bordetella
Biofilm
Interplay
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
dc.description.none.fl_txt_mv Bordetella bronchiseptica, a respiratory pathogen capable of infecting various mammals, including humans, is associated with chronic infections, contrasting with the acute infections caused by B. pertussis. Both pathogens can form biofilm-like structures in vivo, providing tolerance against environmental stresses. Biofilm formation in B. bronchiseptica is regulated by the BvgAS two-component system, with intermediate concentrations of certain modulators inducing a phase favoring biofilm formation. Recent studies have highlighted the role of cyclic diguanylate monophosphate (c-di-GMP) in this process: elevated c-di-GMP levels stimulate biofilm formation, whereas phosphodiesterase (PDE) activation reduces biofilms. Respiratory secretions, which contain albumin and calcium at higher concentrations than standard growth media, promote an increase in the amount and localization of the adenylate cyclase toxin (AC), an important Bordetella virulence factor. Secreted AC present in the extracellular media or attached to the outer membrane inhibits biofilm formation. Based on these observations, we hypothesized that serum albumin and calcium inhibit biofilm formation and explored the involvement of c-di-GMP in this process. Our findings demonstrate that albumin and calcium inhibit B. bronchiseptica biofilm formation by two apparently independent mechanisms, formation, increasing with AC secretion playing a significant role, while the filamentous hemagglutinin adhesin (FHA) does not appear to be directly involved. Furthermore,and inducing c-di-GMP degradation. regulates biofilm formation in response to albumin and calcium. This study enhances our understanding of the complex mechanisms governing B. bronchiseptica biofilm formation and its modulation by host factors.
Fil: Mugni, Sabrina Laura. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Argentina. Fil: Ambrosis, Nicolás Martín. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Argentina. Fil: O'Toole, George A. Geisel School of Medicine at Dartmouth, Hanover. Department of Microbiology and Immunology. Estados Unidos. Fil: Sisti, Federico. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Argentina. Fil: Fernández, Julieta. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Argentina.
Instituto de Biotecnología y Biología Molecular
description Bordetella bronchiseptica, a respiratory pathogen capable of infecting various mammals, including humans, is associated with chronic infections, contrasting with the acute infections caused by B. pertussis. Both pathogens can form biofilm-like structures in vivo, providing tolerance against environmental stresses. Biofilm formation in B. bronchiseptica is regulated by the BvgAS two-component system, with intermediate concentrations of certain modulators inducing a phase favoring biofilm formation. Recent studies have highlighted the role of cyclic diguanylate monophosphate (c-di-GMP) in this process: elevated c-di-GMP levels stimulate biofilm formation, whereas phosphodiesterase (PDE) activation reduces biofilms. Respiratory secretions, which contain albumin and calcium at higher concentrations than standard growth media, promote an increase in the amount and localization of the adenylate cyclase toxin (AC), an important Bordetella virulence factor. Secreted AC present in the extracellular media or attached to the outer membrane inhibits biofilm formation. Based on these observations, we hypothesized that serum albumin and calcium inhibit biofilm formation and explored the involvement of c-di-GMP in this process. Our findings demonstrate that albumin and calcium inhibit B. bronchiseptica biofilm formation by two apparently independent mechanisms, formation, increasing with AC secretion playing a significant role, while the filamentous hemagglutinin adhesin (FHA) does not appear to be directly involved. Furthermore,and inducing c-di-GMP degradation. regulates biofilm formation in response to albumin and calcium. This study enhances our understanding of the complex mechanisms governing B. bronchiseptica biofilm formation and its modulation by host factors.
publishDate 2025
dc.date.none.fl_str_mv 2025
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