Immunomodulatory effects of Escherichia coli ATCC 25922 on allergic airway inflammation in a mouse model.

<h4>Background</h4>Hygiene hypothesis demonstrates that the lack of microbial exposure would promote the development of allergic airway disease (AAD). Therefore, the gut microbiota, including Escherichia coli (E. coli), would probably offer a potential strategy for AAD.<h4>Objectiv...

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Autores principales: Wenhui Pang, Hefeng Wang, Lei Shi, Yueqi Sun, Xiaoting Wang, Mingming Wang, Jianfeng Li, Haibo Wang, Guanggang Shi
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Publicado: Public Library of Science (PLoS) 2013
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spelling oai:doaj.org-article:84035a56aa7643f991093f3bfa2bb0392021-11-18T07:52:09ZImmunomodulatory effects of Escherichia coli ATCC 25922 on allergic airway inflammation in a mouse model.1932-620310.1371/journal.pone.0059174https://doaj.org/article/84035a56aa7643f991093f3bfa2bb0392013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23536867/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Hygiene hypothesis demonstrates that the lack of microbial exposure would promote the development of allergic airway disease (AAD). Therefore, the gut microbiota, including Escherichia coli (E. coli), would probably offer a potential strategy for AAD.<h4>Objective</h4>To investigate whether E. coli infection is able to suppress the induction of AAD and to elucidate the underlying mechanisms.<h4>Methods</h4>Nonpathogenic E. coli ATCC 25922 was infected by gavage before AAD phase in three patterns: 10(8) or 10(6) CFU in neonates or 10(8) CFU in adults. Then mice were sensitized and challenged with ovalbumin (OVA) to induce allergic inflammation in both the upper and lower airways. Hallmarks of AAD, in terms of eosinophil infiltration and goblet cell metaplasia in subepithelial mucosa, Th2 skewing of the immune response, and levels of T regulate cells (Tregs), were examined by histological analysis, ELISA, and flow cytometry, respectively.<h4>Results</h4>E. coli, especially neonatally infected with an optimal dose, attenuated allergic responses, including a decrease in nasal rubbing and sneezing, a reduction in eosinophil inflammation and goblet cell metaplasia in subepithelial mucosa, decreased serum levels of OVA-specific IgE, and reduced Th2 (IL-4) cytokines. In contrast, this effect came with an increase of Th1 (IFN-r and IL-2) cytokines, and an enhancement of IL-10-secreting Tregs in paratracheal lymph nodes (PTLN).<h4>Conclusion</h4>E. coli suppresses allergic responses in mice, probably via a shift from Th1 to Th2 and/or induction of Tregs. Moreover, this infection is age- and dose-dependent, which may open up novel possibilities for new therapeutic interventions.Wenhui PangHefeng WangLei ShiYueqi SunXiaoting WangMingming WangJianfeng LiHaibo WangGuanggang ShiPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 3, p e59174 (2013)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Wenhui Pang
Hefeng Wang
Lei Shi
Yueqi Sun
Xiaoting Wang
Mingming Wang
Jianfeng Li
Haibo Wang
Guanggang Shi
Immunomodulatory effects of Escherichia coli ATCC 25922 on allergic airway inflammation in a mouse model.
description <h4>Background</h4>Hygiene hypothesis demonstrates that the lack of microbial exposure would promote the development of allergic airway disease (AAD). Therefore, the gut microbiota, including Escherichia coli (E. coli), would probably offer a potential strategy for AAD.<h4>Objective</h4>To investigate whether E. coli infection is able to suppress the induction of AAD and to elucidate the underlying mechanisms.<h4>Methods</h4>Nonpathogenic E. coli ATCC 25922 was infected by gavage before AAD phase in three patterns: 10(8) or 10(6) CFU in neonates or 10(8) CFU in adults. Then mice were sensitized and challenged with ovalbumin (OVA) to induce allergic inflammation in both the upper and lower airways. Hallmarks of AAD, in terms of eosinophil infiltration and goblet cell metaplasia in subepithelial mucosa, Th2 skewing of the immune response, and levels of T regulate cells (Tregs), were examined by histological analysis, ELISA, and flow cytometry, respectively.<h4>Results</h4>E. coli, especially neonatally infected with an optimal dose, attenuated allergic responses, including a decrease in nasal rubbing and sneezing, a reduction in eosinophil inflammation and goblet cell metaplasia in subepithelial mucosa, decreased serum levels of OVA-specific IgE, and reduced Th2 (IL-4) cytokines. In contrast, this effect came with an increase of Th1 (IFN-r and IL-2) cytokines, and an enhancement of IL-10-secreting Tregs in paratracheal lymph nodes (PTLN).<h4>Conclusion</h4>E. coli suppresses allergic responses in mice, probably via a shift from Th1 to Th2 and/or induction of Tregs. Moreover, this infection is age- and dose-dependent, which may open up novel possibilities for new therapeutic interventions.
format article
author Wenhui Pang
Hefeng Wang
Lei Shi
Yueqi Sun
Xiaoting Wang
Mingming Wang
Jianfeng Li
Haibo Wang
Guanggang Shi
author_facet Wenhui Pang
Hefeng Wang
Lei Shi
Yueqi Sun
Xiaoting Wang
Mingming Wang
Jianfeng Li
Haibo Wang
Guanggang Shi
author_sort Wenhui Pang
title Immunomodulatory effects of Escherichia coli ATCC 25922 on allergic airway inflammation in a mouse model.
title_short Immunomodulatory effects of Escherichia coli ATCC 25922 on allergic airway inflammation in a mouse model.
title_full Immunomodulatory effects of Escherichia coli ATCC 25922 on allergic airway inflammation in a mouse model.
title_fullStr Immunomodulatory effects of Escherichia coli ATCC 25922 on allergic airway inflammation in a mouse model.
title_full_unstemmed Immunomodulatory effects of Escherichia coli ATCC 25922 on allergic airway inflammation in a mouse model.
title_sort immunomodulatory effects of escherichia coli atcc 25922 on allergic airway inflammation in a mouse model.
publisher Public Library of Science (PLoS)
publishDate 2013
url https://doaj.org/article/84035a56aa7643f991093f3bfa2bb039
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