Selective effects of Liver X Receptor activation in host-bacteria interaction

Macrophages exert potent microbicidal functions against pathogens; however, some intracellular bacteria have developed strategies to survive within intracellular phagolysosomes and use macrophages as a preferential niche to replicate. Liver X receptors (LXRs) are ligand- activated transcription fact...

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Detalles Bibliográficos
Autor: Glaría Percaz, Estibaliz
Tipo de recurso: tesis doctoral
Estado:Versión publicada
Fecha de publicación:2021
País:España
Institución:CBUC, CESCA
Repositorio:TDR. Tesis Doctorales en Red
OAI Identifier:oai:www.tdx.cat:10803/673708
Acceso en línea:http://hdl.handle.net/10803/673708
Access Level:acceso abierto
Palabra clave:Sistema immunitari
Sistema inmunológico
Immune system
Macròfags
Macrófagos
Macrophages
Metabolisme
Metabolismo
Metabolism
Bacteris
Bacterias
Bacteria
Receptors cel·lulars
Receptores celulares
Cell receptors
Fetge
Hígado
Liver
Ciències Experimentals i Matemàtiques
577
id ES_dc7dd94d22aba408ea22394f438debaa
oai_identifier_str oai:www.tdx.cat:10803/673708
network_acronym_str ES
network_name_str España
repository_id_str
dc.title.none.fl_str_mv Selective effects of Liver X Receptor activation in host-bacteria interaction
title Selective effects of Liver X Receptor activation in host-bacteria interaction
spellingShingle Selective effects of Liver X Receptor activation in host-bacteria interaction
Glaría Percaz, Estibaliz
Sistema immunitari
Sistema inmunológico
Immune system
Macròfags
Macrófagos
Macrophages
Metabolisme
Metabolismo
Metabolism
Bacteris
Bacterias
Bacteria
Receptors cel·lulars
Receptores celulares
Cell receptors
Fetge
Hígado
Liver
Ciències Experimentals i Matemàtiques
577
title_short Selective effects of Liver X Receptor activation in host-bacteria interaction
title_full Selective effects of Liver X Receptor activation in host-bacteria interaction
title_fullStr Selective effects of Liver X Receptor activation in host-bacteria interaction
title_full_unstemmed Selective effects of Liver X Receptor activation in host-bacteria interaction
title_sort Selective effects of Liver X Receptor activation in host-bacteria interaction
dc.creator.none.fl_str_mv Glaría Percaz, Estibaliz
author Glaría Percaz, Estibaliz
author_facet Glaría Percaz, Estibaliz
author_role author
dc.contributor.none.fl_str_mv Valledor Fernández, Annabel
Valledor Fernández, Annabel
Universitat de Barcelona. Departament de Biologia Cel·lular, Fisiologia i Immunologia
dc.subject.none.fl_str_mv Sistema immunitari
Sistema inmunológico
Immune system
Macròfags
Macrófagos
Macrophages
Metabolisme
Metabolismo
Metabolism
Bacteris
Bacterias
Bacteria
Receptors cel·lulars
Receptores celulares
Cell receptors
Fetge
Hígado
Liver
Ciències Experimentals i Matemàtiques
577
topic Sistema immunitari
Sistema inmunológico
Immune system
Macròfags
Macrófagos
Macrophages
Metabolisme
Metabolismo
Metabolism
Bacteris
Bacterias
Bacteria
Receptors cel·lulars
Receptores celulares
Cell receptors
Fetge
Hígado
Liver
Ciències Experimentals i Matemàtiques
577
description Macrophages exert potent microbicidal functions against pathogens; however, some intracellular bacteria have developed strategies to survive within intracellular phagolysosomes and use macrophages as a preferential niche to replicate. Liver X receptors (LXRs) are ligand- activated transcription factors of the nuclear receptor superfamily that regulate metabolic and immune functions. In this study, we explored the impact of LXR activation on host–bacteria interactions and its consequences on infection. In a murine model of orally-acquired salmonellosis, the pharmacological activation of LXRs reduced extraintestinal bacterial dissemination and attenuated the clinical signs of infection. The beneficial effects of LXR activation in the control of infection required the expression of the multifunctional protein CD38 in bone marrow-derived cells. We had previously described CD38 as a new LXR target gene that is synergistically induced by the combination of LXR agonists and inflammatory stimuli in macrophages. Here, we have identified the transcription factor C/EBPβ as an essential mediator of Cd38 induction by TNFα, IFNγ, or LPS, as well as by the combination of these inflammatory signals and an LXR agonist. In murine macrophages, LXR activation reduced the internalisation of Salmonella Typhimurium, uropathogenic E. coli, and enteroinvasive E. coli (EIEC) but not of Listeria monocytogenes, Staphylococcus aureus, or latex microspheres. After analysing several LXR-mediated activities, we found that S. Typhimurium infection correlated with the abundance of free cholesterol in macrophages, indicating that the reduction in cellular cholesterol caused by LXR activation might mediate the inhibitory effect on bacterial entry. In primary human macrophages, LXR activation reduced the infection by S. Typhimurium but not by EIEC or S. aureus. Strikingly, LXR activation caused either no effect or a reduction in the internalisation of L. monocytogenes and latex microspheres depending on the donor. In conclusion, this work delves into the mechanisms by which LXRs modulate host interactions with bacteria. Given that the ability of many bacteria to invade host cells largely depends on initial surface contacts, modulating these events through LXR-targeting compounds opens new potential therapeutic opportunities for antibacterial drug development.
publishDate 2021
dc.date.none.fl_str_mv 2021
2022
2022
dc.type.none.fl_str_mv info:eu-repo/semantics/doctoralThesis
info:eu-repo/semantics/publishedVersion
format doctoralThesis
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/10803/673708
url http://hdl.handle.net/10803/673708
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 238 p.
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Universitat de Barcelona
publisher.none.fl_str_mv Universitat de Barcelona
dc.source.none.fl_str_mv TDX (Tesis Doctorals en Xarxa)
reponame:TDR. Tesis Doctorales en Red
instname:CBUC, CESCA
instname_str CBUC, CESCA
reponame_str TDR. Tesis Doctorales en Red
collection TDR. Tesis Doctorales en Red
repository.name.fl_str_mv
repository.mail.fl_str_mv
_version_ 1869421773852770304
spelling Selective effects of Liver X Receptor activation in host-bacteria interactionGlaría Percaz, EstibalizSistema immunitariSistema inmunológicoImmune systemMacròfagsMacrófagosMacrophagesMetabolismeMetabolismoMetabolismBacterisBacteriasBacteriaReceptors cel·lularsReceptores celularesCell receptorsFetgeHígadoLiverCiències Experimentals i Matemàtiques577Macrophages exert potent microbicidal functions against pathogens; however, some intracellular bacteria have developed strategies to survive within intracellular phagolysosomes and use macrophages as a preferential niche to replicate. Liver X receptors (LXRs) are ligand- activated transcription factors of the nuclear receptor superfamily that regulate metabolic and immune functions. In this study, we explored the impact of LXR activation on host–bacteria interactions and its consequences on infection. In a murine model of orally-acquired salmonellosis, the pharmacological activation of LXRs reduced extraintestinal bacterial dissemination and attenuated the clinical signs of infection. The beneficial effects of LXR activation in the control of infection required the expression of the multifunctional protein CD38 in bone marrow-derived cells. We had previously described CD38 as a new LXR target gene that is synergistically induced by the combination of LXR agonists and inflammatory stimuli in macrophages. Here, we have identified the transcription factor C/EBPβ as an essential mediator of Cd38 induction by TNFα, IFNγ, or LPS, as well as by the combination of these inflammatory signals and an LXR agonist. In murine macrophages, LXR activation reduced the internalisation of Salmonella Typhimurium, uropathogenic E. coli, and enteroinvasive E. coli (EIEC) but not of Listeria monocytogenes, Staphylococcus aureus, or latex microspheres. After analysing several LXR-mediated activities, we found that S. Typhimurium infection correlated with the abundance of free cholesterol in macrophages, indicating that the reduction in cellular cholesterol caused by LXR activation might mediate the inhibitory effect on bacterial entry. In primary human macrophages, LXR activation reduced the infection by S. Typhimurium but not by EIEC or S. aureus. Strikingly, LXR activation caused either no effect or a reduction in the internalisation of L. monocytogenes and latex microspheres depending on the donor. In conclusion, this work delves into the mechanisms by which LXRs modulate host interactions with bacteria. Given that the ability of many bacteria to invade host cells largely depends on initial surface contacts, modulating these events through LXR-targeting compounds opens new potential therapeutic opportunities for antibacterial drug development.Universitat de BarcelonaValledor Fernández, AnnabelValledor Fernández, AnnabelUniversitat de Barcelona. Departament de Biologia Cel·lular, Fisiologia i Immunologia202220222021info:eu-repo/semantics/doctoralThesisinfo:eu-repo/semantics/publishedVersion238 p.application/pdfapplication/pdfhttp://hdl.handle.net/10803/673708TDX (Tesis Doctorals en Xarxa)reponame:TDR. Tesis Doctorales en Redinstname:CBUC, CESCAInglésADVERTIMENT. Tots els drets reservats. L'accés als continguts d'aquesta tesi doctoral i la seva utilització ha de respectar els drets de la persona autora. Pot ser utilitzada per a consulta o estudi personal, així com en activitats o materials d'investigació i docència en els termes establerts a l'art. 32 del Text Refós de la Llei de Propietat Intel·lectual (RDL 1/1996). Per altres utilitzacions es requereix l'autorització prèvia i expressa de la persona autora. En qualsevol cas, en la utilització dels seus continguts caldrà indicar de forma clara el nom i cognoms de la persona autora i el títol de la tesi doctoral. No s'autoritza la seva reproducció o altres formes d'explotació efectuades amb finalitats de lucre ni la seva comunicació pública des d'un lloc aliè al servei TDX. Tampoc s'autoritza la presentació del seu contingut en una finestra o marc aliè a TDX (framing). Aquesta reserva de drets afecta tant als continguts de la tesi com als seus resums i índexs.info:eu-repo/semantics/openAccessoai:www.tdx.cat:10803/6737082026-06-14T12:46:07Z
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