Effect of antibiotic gut microbiota disruption on LPS-induced acute lung inflammation.


Journal

PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081

Informations de publication

Date de publication:
2020
Historique:
received: 12 05 2020
accepted: 21 10 2020
entrez: 4 11 2020
pubmed: 5 11 2020
medline: 29 12 2020
Statut: epublish

Résumé

An increasing body of evidence is indicating that the gut microbiota modulates pulmonary inflammatory responses. This so-called gut-lung axis might be of importance in a whole spectrum of inflammatory pulmonary diseases such as acute respiratory distress syndrome, chronic obstructive pulmonary disease and pneumonia. Here, we investigate the effect of antibiotic disruption of gut microbiota on immune responses in the lung after a intranasal challenge with lipopolysaccharide (LPS). C57Bl/6 mice were treated for two weeks with broad-spectrum antibiotics supplemented to their drinking water. Afterwards, mice and untreated control mice were inoculated intranasally with LPS. Mice were sacrificed 2 and 6 hours post-challenge, after which bronchoalveolar lavage fluid (BALF) and lung tissues were taken. Gut microbiota analysis showed that antibiotic-treated mice had a pronounced reduction in numbers and diversity of bacteria. A modest, but time consistent, significant increase of interleukin (IL)-6 release was seen in BALF of antibiotic treated mice. Release of tumor necrosis factor alpha (TNFα), however, was not statistically different between groups. Antibiotic induced microbiota disruption is associated with alterations in host responses during LPS-induced lung inflammation. Further studies are required to determine the clinical relevance of the gut-lung axis in pulmonary infection and inflammation.

Sections du résumé

BACKGROUND
An increasing body of evidence is indicating that the gut microbiota modulates pulmonary inflammatory responses. This so-called gut-lung axis might be of importance in a whole spectrum of inflammatory pulmonary diseases such as acute respiratory distress syndrome, chronic obstructive pulmonary disease and pneumonia. Here, we investigate the effect of antibiotic disruption of gut microbiota on immune responses in the lung after a intranasal challenge with lipopolysaccharide (LPS).
METHODS/RESULTS
C57Bl/6 mice were treated for two weeks with broad-spectrum antibiotics supplemented to their drinking water. Afterwards, mice and untreated control mice were inoculated intranasally with LPS. Mice were sacrificed 2 and 6 hours post-challenge, after which bronchoalveolar lavage fluid (BALF) and lung tissues were taken. Gut microbiota analysis showed that antibiotic-treated mice had a pronounced reduction in numbers and diversity of bacteria. A modest, but time consistent, significant increase of interleukin (IL)-6 release was seen in BALF of antibiotic treated mice. Release of tumor necrosis factor alpha (TNFα), however, was not statistically different between groups.
CONCLUSION
Antibiotic induced microbiota disruption is associated with alterations in host responses during LPS-induced lung inflammation. Further studies are required to determine the clinical relevance of the gut-lung axis in pulmonary infection and inflammation.

Identifiants

pubmed: 33147273
doi: 10.1371/journal.pone.0241748
pii: PONE-D-20-14015
pmc: PMC7641457
doi:

Substances chimiques

Anti-Bacterial Agents 0
Interleukin-6 0
Lipopolysaccharides 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e0241748

Déclaration de conflit d'intérêts

The authors have declared that no competing interests exist.

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Auteurs

Max C Jacobs (MC)

Center for Experimental and Molecular Medicine, Amsterdam UMC, Location Academic Medical Center (AMC), Amsterdam Infection & Immunity Institute, University of Amsterdam, Amsterdam, The Netherlands.

Jacqueline M Lankelma (JM)

Center for Experimental and Molecular Medicine, Amsterdam UMC, Location Academic Medical Center (AMC), Amsterdam Infection & Immunity Institute, University of Amsterdam, Amsterdam, The Netherlands.

Nora S Wolff (NS)

Center for Experimental and Molecular Medicine, Amsterdam UMC, Location Academic Medical Center (AMC), Amsterdam Infection & Immunity Institute, University of Amsterdam, Amsterdam, The Netherlands.

Floor Hugenholtz (F)

Center for Experimental and Molecular Medicine, Amsterdam UMC, Location Academic Medical Center (AMC), Amsterdam Infection & Immunity Institute, University of Amsterdam, Amsterdam, The Netherlands.

Alex F de Vos (AF)

Center for Experimental and Molecular Medicine, Amsterdam UMC, Location Academic Medical Center (AMC), Amsterdam Infection & Immunity Institute, University of Amsterdam, Amsterdam, The Netherlands.

Tom van der Poll (T)

Center for Experimental and Molecular Medicine, Amsterdam UMC, Location Academic Medical Center (AMC), Amsterdam Infection & Immunity Institute, University of Amsterdam, Amsterdam, The Netherlands.
Division of Infectious Diseases, Department of Medicine, Amsterdam UMC, Location Academic Medical Center (AMC), Amsterdam Infection & Immunity Institute, University of Amsterdam, Amsterdam, The Netherlands.

W Joost Wiersinga (WJ)

Center for Experimental and Molecular Medicine, Amsterdam UMC, Location Academic Medical Center (AMC), Amsterdam Infection & Immunity Institute, University of Amsterdam, Amsterdam, The Netherlands.
Division of Infectious Diseases, Department of Medicine, Amsterdam UMC, Location Academic Medical Center (AMC), Amsterdam Infection & Immunity Institute, University of Amsterdam, Amsterdam, The Netherlands.

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