Antibiotic use during pregnancy is linked to offspring gut microbial dysbiosis, barrier disruption, and altered immunity along the gut–lung axis
- Autores
- Alhasan, Moumen M.; Hölsken, Oliver; Duerr, Claudia; Helfrich, Sofia; Branzk, Nora; Philipp, Alina; Leitz, Dominik; Duerr, Julia; Almousa, Yahia; Barrientos, Gabriela Laura; Mohn, William W.; Gamradt, Stefanie; Conrad, Melanie L.
- Año de publicación
- 2023
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Antibiotic use during pregnancy is associated with increased asthma risk in children. Since approximately 25% of women use antibiotics during pregnancy, it is important to identify the pathways involved in this phenomenon. We investigate how mother-to-offspring transfer of antibiotic-induced gut microbial dysbiosis influences immune system development along the gut–lung axis. Using a mouse model of maternal antibiotic exposure during pregnancy, we immunophenotyped offspring in early life and after asthma induction. In early life, prenatal-antibiotic exposed offspring exhibited gut microbial dysbiosis, intestinal inflammation (increased fecal lipocalin-2 and IgA), and dysregulated intestinal ILC3 subtypes. Intestinal barrier dysfunction in the offspring was indicated by a FITC-dextran intestinal permeability assay and circulating lipopolysaccharide. This was accompanied by increased T-helper (Th)17 cell percentages in the offspring's blood and lungs in both early life and after allergy induction. Lung tissue additionally showed increased percentages of RORγt T-regulatory (Treg) cells at both time points. Our investigation of the gut–lung axis identifies early-life gut dysbiosis, intestinal inflammation, and barrier dysfunction as a possible developmental programming event promoting increased expression of RORγt in blood and lung CD4+ T cells that may contribute to increased asthma risk.
Fil: Alhasan, Moumen M.. Universität zu Berlin; Alemania
Fil: Hölsken, Oliver. Freie Universität Berlin; Alemania
Fil: Duerr, Claudia. Freie Universität Berlin; Alemania
Fil: Helfrich, Sofia. Freie Universität Berlin; Alemania
Fil: Branzk, Nora. Freie Universität Berlin; Alemania
Fil: Philipp, Alina. Freie Universität Berlin; Alemania
Fil: Leitz, Dominik. Freie Universität Berlin; Alemania
Fil: Duerr, Julia. Freie Universität Berlin; Alemania
Fil: Almousa, Yahia. Freie Universität Berlin; Alemania
Fil: Barrientos, Gabriela Laura. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Hospital Aleman; Argentina
Fil: Mohn, William W.. University of British Columbia; Canadá
Fil: Gamradt, Stefanie. Freie Universität Berlin; Alemania
Fil: Conrad, Melanie L.. Freie Universität Berlin; Alemania - Materia
-
ANTIBIOTICS
ASTHMA
GUT–LUNG AXIS
PREGNANCY
TH17 CELL - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/219931
Ver los metadatos del registro completo
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oai:ri.conicet.gov.ar:11336/219931 |
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network_name_str |
CONICET Digital (CONICET) |
spelling |
Antibiotic use during pregnancy is linked to offspring gut microbial dysbiosis, barrier disruption, and altered immunity along the gut–lung axisAlhasan, Moumen M.Hölsken, OliverDuerr, ClaudiaHelfrich, SofiaBranzk, NoraPhilipp, AlinaLeitz, DominikDuerr, JuliaAlmousa, YahiaBarrientos, Gabriela LauraMohn, William W.Gamradt, StefanieConrad, Melanie L.ANTIBIOTICSASTHMAGUT–LUNG AXISPREGNANCYTH17 CELLhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Antibiotic use during pregnancy is associated with increased asthma risk in children. Since approximately 25% of women use antibiotics during pregnancy, it is important to identify the pathways involved in this phenomenon. We investigate how mother-to-offspring transfer of antibiotic-induced gut microbial dysbiosis influences immune system development along the gut–lung axis. Using a mouse model of maternal antibiotic exposure during pregnancy, we immunophenotyped offspring in early life and after asthma induction. In early life, prenatal-antibiotic exposed offspring exhibited gut microbial dysbiosis, intestinal inflammation (increased fecal lipocalin-2 and IgA), and dysregulated intestinal ILC3 subtypes. Intestinal barrier dysfunction in the offspring was indicated by a FITC-dextran intestinal permeability assay and circulating lipopolysaccharide. This was accompanied by increased T-helper (Th)17 cell percentages in the offspring's blood and lungs in both early life and after allergy induction. Lung tissue additionally showed increased percentages of RORγt T-regulatory (Treg) cells at both time points. Our investigation of the gut–lung axis identifies early-life gut dysbiosis, intestinal inflammation, and barrier dysfunction as a possible developmental programming event promoting increased expression of RORγt in blood and lung CD4+ T cells that may contribute to increased asthma risk.Fil: Alhasan, Moumen M.. Universität zu Berlin; AlemaniaFil: Hölsken, Oliver. Freie Universität Berlin; AlemaniaFil: Duerr, Claudia. Freie Universität Berlin; AlemaniaFil: Helfrich, Sofia. Freie Universität Berlin; AlemaniaFil: Branzk, Nora. Freie Universität Berlin; AlemaniaFil: Philipp, Alina. Freie Universität Berlin; AlemaniaFil: Leitz, Dominik. Freie Universität Berlin; AlemaniaFil: Duerr, Julia. Freie Universität Berlin; AlemaniaFil: Almousa, Yahia. Freie Universität Berlin; AlemaniaFil: Barrientos, Gabriela Laura. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Hospital Aleman; ArgentinaFil: Mohn, William W.. University of British Columbia; CanadáFil: Gamradt, Stefanie. Freie Universität Berlin; AlemaniaFil: Conrad, Melanie L.. Freie Universität Berlin; AlemaniaWiley VCH Verlag2023-07info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/219931Alhasan, Moumen M.; Hölsken, Oliver; Duerr, Claudia; Helfrich, Sofia; Branzk, Nora; et al.; Antibiotic use during pregnancy is linked to offspring gut microbial dysbiosis, barrier disruption, and altered immunity along the gut–lung axis; Wiley VCH Verlag; European Journal of Immunology; 53; 10; 7-2023; 1-150014-2980CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1002/eji.202350394info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:39:59Zoai:ri.conicet.gov.ar:11336/219931instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 10:39:59.726CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
Antibiotic use during pregnancy is linked to offspring gut microbial dysbiosis, barrier disruption, and altered immunity along the gut–lung axis |
title |
Antibiotic use during pregnancy is linked to offspring gut microbial dysbiosis, barrier disruption, and altered immunity along the gut–lung axis |
spellingShingle |
Antibiotic use during pregnancy is linked to offspring gut microbial dysbiosis, barrier disruption, and altered immunity along the gut–lung axis Alhasan, Moumen M. ANTIBIOTICS ASTHMA GUT–LUNG AXIS PREGNANCY TH17 CELL |
title_short |
Antibiotic use during pregnancy is linked to offspring gut microbial dysbiosis, barrier disruption, and altered immunity along the gut–lung axis |
title_full |
Antibiotic use during pregnancy is linked to offspring gut microbial dysbiosis, barrier disruption, and altered immunity along the gut–lung axis |
title_fullStr |
Antibiotic use during pregnancy is linked to offspring gut microbial dysbiosis, barrier disruption, and altered immunity along the gut–lung axis |
title_full_unstemmed |
Antibiotic use during pregnancy is linked to offspring gut microbial dysbiosis, barrier disruption, and altered immunity along the gut–lung axis |
title_sort |
Antibiotic use during pregnancy is linked to offspring gut microbial dysbiosis, barrier disruption, and altered immunity along the gut–lung axis |
dc.creator.none.fl_str_mv |
Alhasan, Moumen M. Hölsken, Oliver Duerr, Claudia Helfrich, Sofia Branzk, Nora Philipp, Alina Leitz, Dominik Duerr, Julia Almousa, Yahia Barrientos, Gabriela Laura Mohn, William W. Gamradt, Stefanie Conrad, Melanie L. |
author |
Alhasan, Moumen M. |
author_facet |
Alhasan, Moumen M. Hölsken, Oliver Duerr, Claudia Helfrich, Sofia Branzk, Nora Philipp, Alina Leitz, Dominik Duerr, Julia Almousa, Yahia Barrientos, Gabriela Laura Mohn, William W. Gamradt, Stefanie Conrad, Melanie L. |
author_role |
author |
author2 |
Hölsken, Oliver Duerr, Claudia Helfrich, Sofia Branzk, Nora Philipp, Alina Leitz, Dominik Duerr, Julia Almousa, Yahia Barrientos, Gabriela Laura Mohn, William W. Gamradt, Stefanie Conrad, Melanie L. |
author2_role |
author author author author author author author author author author author author |
dc.subject.none.fl_str_mv |
ANTIBIOTICS ASTHMA GUT–LUNG AXIS PREGNANCY TH17 CELL |
topic |
ANTIBIOTICS ASTHMA GUT–LUNG AXIS PREGNANCY TH17 CELL |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3 |
dc.description.none.fl_txt_mv |
Antibiotic use during pregnancy is associated with increased asthma risk in children. Since approximately 25% of women use antibiotics during pregnancy, it is important to identify the pathways involved in this phenomenon. We investigate how mother-to-offspring transfer of antibiotic-induced gut microbial dysbiosis influences immune system development along the gut–lung axis. Using a mouse model of maternal antibiotic exposure during pregnancy, we immunophenotyped offspring in early life and after asthma induction. In early life, prenatal-antibiotic exposed offspring exhibited gut microbial dysbiosis, intestinal inflammation (increased fecal lipocalin-2 and IgA), and dysregulated intestinal ILC3 subtypes. Intestinal barrier dysfunction in the offspring was indicated by a FITC-dextran intestinal permeability assay and circulating lipopolysaccharide. This was accompanied by increased T-helper (Th)17 cell percentages in the offspring's blood and lungs in both early life and after allergy induction. Lung tissue additionally showed increased percentages of RORγt T-regulatory (Treg) cells at both time points. Our investigation of the gut–lung axis identifies early-life gut dysbiosis, intestinal inflammation, and barrier dysfunction as a possible developmental programming event promoting increased expression of RORγt in blood and lung CD4+ T cells that may contribute to increased asthma risk. Fil: Alhasan, Moumen M.. Universität zu Berlin; Alemania Fil: Hölsken, Oliver. Freie Universität Berlin; Alemania Fil: Duerr, Claudia. Freie Universität Berlin; Alemania Fil: Helfrich, Sofia. Freie Universität Berlin; Alemania Fil: Branzk, Nora. Freie Universität Berlin; Alemania Fil: Philipp, Alina. Freie Universität Berlin; Alemania Fil: Leitz, Dominik. Freie Universität Berlin; Alemania Fil: Duerr, Julia. Freie Universität Berlin; Alemania Fil: Almousa, Yahia. Freie Universität Berlin; Alemania Fil: Barrientos, Gabriela Laura. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Hospital Aleman; Argentina Fil: Mohn, William W.. University of British Columbia; Canadá Fil: Gamradt, Stefanie. Freie Universität Berlin; Alemania Fil: Conrad, Melanie L.. Freie Universität Berlin; Alemania |
description |
Antibiotic use during pregnancy is associated with increased asthma risk in children. Since approximately 25% of women use antibiotics during pregnancy, it is important to identify the pathways involved in this phenomenon. We investigate how mother-to-offspring transfer of antibiotic-induced gut microbial dysbiosis influences immune system development along the gut–lung axis. Using a mouse model of maternal antibiotic exposure during pregnancy, we immunophenotyped offspring in early life and after asthma induction. In early life, prenatal-antibiotic exposed offspring exhibited gut microbial dysbiosis, intestinal inflammation (increased fecal lipocalin-2 and IgA), and dysregulated intestinal ILC3 subtypes. Intestinal barrier dysfunction in the offspring was indicated by a FITC-dextran intestinal permeability assay and circulating lipopolysaccharide. This was accompanied by increased T-helper (Th)17 cell percentages in the offspring's blood and lungs in both early life and after allergy induction. Lung tissue additionally showed increased percentages of RORγt T-regulatory (Treg) cells at both time points. Our investigation of the gut–lung axis identifies early-life gut dysbiosis, intestinal inflammation, and barrier dysfunction as a possible developmental programming event promoting increased expression of RORγt in blood and lung CD4+ T cells that may contribute to increased asthma risk. |
publishDate |
2023 |
dc.date.none.fl_str_mv |
2023-07 |
dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
format |
article |
status_str |
publishedVersion |
dc.identifier.none.fl_str_mv |
http://hdl.handle.net/11336/219931 Alhasan, Moumen M.; Hölsken, Oliver; Duerr, Claudia; Helfrich, Sofia; Branzk, Nora; et al.; Antibiotic use during pregnancy is linked to offspring gut microbial dysbiosis, barrier disruption, and altered immunity along the gut–lung axis; Wiley VCH Verlag; European Journal of Immunology; 53; 10; 7-2023; 1-15 0014-2980 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/219931 |
identifier_str_mv |
Alhasan, Moumen M.; Hölsken, Oliver; Duerr, Claudia; Helfrich, Sofia; Branzk, Nora; et al.; Antibiotic use during pregnancy is linked to offspring gut microbial dysbiosis, barrier disruption, and altered immunity along the gut–lung axis; Wiley VCH Verlag; European Journal of Immunology; 53; 10; 7-2023; 1-15 0014-2980 CONICET Digital CONICET |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/doi/10.1002/eji.202350394 |
dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by/2.5/ar/ |
eu_rights_str_mv |
openAccess |
rights_invalid_str_mv |
https://creativecommons.org/licenses/by/2.5/ar/ |
dc.format.none.fl_str_mv |
application/pdf application/pdf |
dc.publisher.none.fl_str_mv |
Wiley VCH Verlag |
publisher.none.fl_str_mv |
Wiley VCH Verlag |
dc.source.none.fl_str_mv |
reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas |
reponame_str |
CONICET Digital (CONICET) |
collection |
CONICET Digital (CONICET) |
instname_str |
Consejo Nacional de Investigaciones Científicas y Técnicas |
repository.name.fl_str_mv |
CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas |
repository.mail.fl_str_mv |
dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
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1844614426632650752 |
score |
13.070432 |