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Docosahexaenoic Acid Inhibits Helicobacter pylori Growth In Vitro and Mice Gastric Mucosa Colonization
H. pylori drug-resistant strains and non-compliance to therapy are the major causes of H. pylori eradication failure. For some bacterial species it has been demonstrated that fatty acids have a growth inhibitory effect. Our main aim was to assess the ability of docosahexaenoic acid (DHA) to inhibit...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3328494/ https://www.ncbi.nlm.nih.gov/pubmed/22529974 http://dx.doi.org/10.1371/journal.pone.0035072 |
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author | Correia, Marta Michel, Valérie Matos, António A. Carvalho, Patrícia Oliveira, Maria J. Ferreira, Rui M. Dillies, Marie-Agnès Huerre, Michel Seruca, Raquel Figueiredo, Ceu Machado, Jose C. Touati, Eliette |
author_facet | Correia, Marta Michel, Valérie Matos, António A. Carvalho, Patrícia Oliveira, Maria J. Ferreira, Rui M. Dillies, Marie-Agnès Huerre, Michel Seruca, Raquel Figueiredo, Ceu Machado, Jose C. Touati, Eliette |
author_sort | Correia, Marta |
collection | PubMed |
description | H. pylori drug-resistant strains and non-compliance to therapy are the major causes of H. pylori eradication failure. For some bacterial species it has been demonstrated that fatty acids have a growth inhibitory effect. Our main aim was to assess the ability of docosahexaenoic acid (DHA) to inhibit H. pylori growth both in vitro and in a mouse model. The effectiveness of standard therapy (ST) in combination with DHA on H. pylori eradication and recurrence prevention success was also investigated. The effects of DHA on H. pylori growth were analyzed in an in vitro dose-response study and n in vivo model. We analized the ability of H. pylori to colonize mice gastric mucosa following DHA, ST or a combination of both treatments. Our data demonstrate that DHA decreases H. pylori growth in vitro in a dose-dependent manner. Furthermore, DHA inhibits H. pylori gastric colonization in vivo as well as decreases mouse gastric mucosa inflammation. Addition of DHA to ST was also associated with lower H. pylori infection recurrence in the mouse model. In conclusion, DHA is an inhibitor of H. pylori growth and its ability to colonize mouse stomach. DHA treatment is also associated with a lower recurrence of H. pylori infection in combination with ST. These observations pave the way to consider DHA as an adjunct agent in H. pylori eradication treatment. |
format | Online Article Text |
id | pubmed-3328494 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-33284942012-04-23 Docosahexaenoic Acid Inhibits Helicobacter pylori Growth In Vitro and Mice Gastric Mucosa Colonization Correia, Marta Michel, Valérie Matos, António A. Carvalho, Patrícia Oliveira, Maria J. Ferreira, Rui M. Dillies, Marie-Agnès Huerre, Michel Seruca, Raquel Figueiredo, Ceu Machado, Jose C. Touati, Eliette PLoS One Research Article H. pylori drug-resistant strains and non-compliance to therapy are the major causes of H. pylori eradication failure. For some bacterial species it has been demonstrated that fatty acids have a growth inhibitory effect. Our main aim was to assess the ability of docosahexaenoic acid (DHA) to inhibit H. pylori growth both in vitro and in a mouse model. The effectiveness of standard therapy (ST) in combination with DHA on H. pylori eradication and recurrence prevention success was also investigated. The effects of DHA on H. pylori growth were analyzed in an in vitro dose-response study and n in vivo model. We analized the ability of H. pylori to colonize mice gastric mucosa following DHA, ST or a combination of both treatments. Our data demonstrate that DHA decreases H. pylori growth in vitro in a dose-dependent manner. Furthermore, DHA inhibits H. pylori gastric colonization in vivo as well as decreases mouse gastric mucosa inflammation. Addition of DHA to ST was also associated with lower H. pylori infection recurrence in the mouse model. In conclusion, DHA is an inhibitor of H. pylori growth and its ability to colonize mouse stomach. DHA treatment is also associated with a lower recurrence of H. pylori infection in combination with ST. These observations pave the way to consider DHA as an adjunct agent in H. pylori eradication treatment. Public Library of Science 2012-04-17 /pmc/articles/PMC3328494/ /pubmed/22529974 http://dx.doi.org/10.1371/journal.pone.0035072 Text en Correia et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Correia, Marta Michel, Valérie Matos, António A. Carvalho, Patrícia Oliveira, Maria J. Ferreira, Rui M. Dillies, Marie-Agnès Huerre, Michel Seruca, Raquel Figueiredo, Ceu Machado, Jose C. Touati, Eliette Docosahexaenoic Acid Inhibits Helicobacter pylori Growth In Vitro and Mice Gastric Mucosa Colonization |
title | Docosahexaenoic Acid Inhibits Helicobacter pylori Growth In Vitro and Mice Gastric Mucosa Colonization |
title_full | Docosahexaenoic Acid Inhibits Helicobacter pylori Growth In Vitro and Mice Gastric Mucosa Colonization |
title_fullStr | Docosahexaenoic Acid Inhibits Helicobacter pylori Growth In Vitro and Mice Gastric Mucosa Colonization |
title_full_unstemmed | Docosahexaenoic Acid Inhibits Helicobacter pylori Growth In Vitro and Mice Gastric Mucosa Colonization |
title_short | Docosahexaenoic Acid Inhibits Helicobacter pylori Growth In Vitro and Mice Gastric Mucosa Colonization |
title_sort | docosahexaenoic acid inhibits helicobacter pylori growth in vitro and mice gastric mucosa colonization |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3328494/ https://www.ncbi.nlm.nih.gov/pubmed/22529974 http://dx.doi.org/10.1371/journal.pone.0035072 |
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