Oral administration of Clostridium butyricum rescues streptomycin-exacerbated respiratory syncytial virus-induced lung inflammation in mice

Changes in the intestinal microbiota indirectly impact the health of mucosa distal to the intestine, particularly the respiratory tract. However, the effects of intestinal microbiota dysbiosis on the regulation of respiratory syncytial virus (RSV) infection are not clear. In this study, we examined...

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Main Authors: Wenwen Zhu, Jia Wang, Na Zhao, Rui Zheng, Dalu Wang, Weiwei Liu, Beixing Liu
Format: Article
Language:English
Published: Taylor & Francis Group 2021-12-01
Series:Virulence
Subjects:
Online Access:http://dx.doi.org/10.1080/21505594.2021.1962137
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author Wenwen Zhu
Jia Wang
Na Zhao
Rui Zheng
Dalu Wang
Weiwei Liu
Beixing Liu
author_facet Wenwen Zhu
Jia Wang
Na Zhao
Rui Zheng
Dalu Wang
Weiwei Liu
Beixing Liu
author_sort Wenwen Zhu
collection DOAJ
description Changes in the intestinal microbiota indirectly impact the health of mucosa distal to the intestine, particularly the respiratory tract. However, the effects of intestinal microbiota dysbiosis on the regulation of respiratory syncytial virus (RSV) infection are not clear. In this study, we examined the effects of altering the intestinal microbiota on the pulmonary immune response against RSV infection. BALB/c mice were treated with streptomycin before infection with RSV to study the altered immune response. The ingestion of streptomycin led to a marked alteration in the intestinal microbiota with a reduced abundance of Lactobacillus and Clostridium genera, followed by greatly aggravated pulmonary inflammation in response to RSV infection. This aggravated inflammation was associated with a dysregulated immune response against RSV infection, characterized by the increased expression of IFN-γ and IL-17 and increased pulmonary M1-like macrophage polarization, and decreased expression of IL-5. Supplementation of Clostridium butyricum (CB) prevented aggravated inflammation and the dysregulated immune response characterized by greater M2 polarization of pulmonary macrophages and decreased release of IFN-γ and IL-17 as well as increased IL-5 levels. Furthermore, in vitro and in vivo experiments identified that butyrate, the main metabolite produced by CB, promoted M2 polarization of macrophages in RSV-infected mice exposed to streptomycin. Together, these results demonstrate the mechanism by which intestinal microbiota modulate the pulmonary immune response to RSV infection.
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spelling doaj.art-1fa7833f776a4e039c0e3757acb4a73e2022-12-22T04:16:18ZengTaylor & Francis GroupVirulence2150-55942150-56082021-12-011212133214810.1080/21505594.2021.19621371962137Oral administration of Clostridium butyricum rescues streptomycin-exacerbated respiratory syncytial virus-induced lung inflammation in miceWenwen Zhu0Jia Wang1Na Zhao2Rui Zheng3Dalu Wang4Weiwei Liu5Beixing Liu6China Medical UniversityChina Medical UniversityChina Medical UniversityChina Medical UniversityChina Medical UniversityChina Medical UniversityChina Medical UniversityChanges in the intestinal microbiota indirectly impact the health of mucosa distal to the intestine, particularly the respiratory tract. However, the effects of intestinal microbiota dysbiosis on the regulation of respiratory syncytial virus (RSV) infection are not clear. In this study, we examined the effects of altering the intestinal microbiota on the pulmonary immune response against RSV infection. BALB/c mice were treated with streptomycin before infection with RSV to study the altered immune response. The ingestion of streptomycin led to a marked alteration in the intestinal microbiota with a reduced abundance of Lactobacillus and Clostridium genera, followed by greatly aggravated pulmonary inflammation in response to RSV infection. This aggravated inflammation was associated with a dysregulated immune response against RSV infection, characterized by the increased expression of IFN-γ and IL-17 and increased pulmonary M1-like macrophage polarization, and decreased expression of IL-5. Supplementation of Clostridium butyricum (CB) prevented aggravated inflammation and the dysregulated immune response characterized by greater M2 polarization of pulmonary macrophages and decreased release of IFN-γ and IL-17 as well as increased IL-5 levels. Furthermore, in vitro and in vivo experiments identified that butyrate, the main metabolite produced by CB, promoted M2 polarization of macrophages in RSV-infected mice exposed to streptomycin. Together, these results demonstrate the mechanism by which intestinal microbiota modulate the pulmonary immune response to RSV infection.http://dx.doi.org/10.1080/21505594.2021.1962137gastrointestinal microbiotarsvimmune responsemacrophagesclostridium butyricumbutyrate
spellingShingle Wenwen Zhu
Jia Wang
Na Zhao
Rui Zheng
Dalu Wang
Weiwei Liu
Beixing Liu
Oral administration of Clostridium butyricum rescues streptomycin-exacerbated respiratory syncytial virus-induced lung inflammation in mice
Virulence
gastrointestinal microbiota
rsv
immune response
macrophages
clostridium butyricum
butyrate
title Oral administration of Clostridium butyricum rescues streptomycin-exacerbated respiratory syncytial virus-induced lung inflammation in mice
title_full Oral administration of Clostridium butyricum rescues streptomycin-exacerbated respiratory syncytial virus-induced lung inflammation in mice
title_fullStr Oral administration of Clostridium butyricum rescues streptomycin-exacerbated respiratory syncytial virus-induced lung inflammation in mice
title_full_unstemmed Oral administration of Clostridium butyricum rescues streptomycin-exacerbated respiratory syncytial virus-induced lung inflammation in mice
title_short Oral administration of Clostridium butyricum rescues streptomycin-exacerbated respiratory syncytial virus-induced lung inflammation in mice
title_sort oral administration of clostridium butyricum rescues streptomycin exacerbated respiratory syncytial virus induced lung inflammation in mice
topic gastrointestinal microbiota
rsv
immune response
macrophages
clostridium butyricum
butyrate
url http://dx.doi.org/10.1080/21505594.2021.1962137
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