Alcohol and tobacco consumption affects bacterial richness in oral cavity mucosa biofilms

Background Today there are more than 2 billion alcohol users and about 1.3 billion tobacco users worldwide. The chronic and heavy use of these two substances is at the heart of numerous diseases and may wreak havoc on the human oral microbiome. This study delves into the changes that alcohol and tob...

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Published inBMC microbiology Vol. 14; no. 1; p. 250
Main Authors Thomas, Andrew Maltez, Gleber-Netto, Frederico Omar, Fernandes, Gustavo Ribeiro, Amorim, Maria, Barbosa, Luisa Fernanda, Francisco, Ana Luisa Noronha, Guerra de Andrade, Arthur, Setubal, João Carlos, Kowalski, Luiz Paulo, Nunes, Diana Noronha, Dias-Neto, Emmanuel
Format Journal Article
LanguageEnglish
Published London BioMed Central 03.10.2014
Springer Nature B.V
Subjects
Online AccessGet full text
ISSN1471-2180
1471-2180
DOI10.1186/s12866-014-0250-2

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Abstract Background Today there are more than 2 billion alcohol users and about 1.3 billion tobacco users worldwide. The chronic and heavy use of these two substances is at the heart of numerous diseases and may wreak havoc on the human oral microbiome. This study delves into the changes that alcohol and tobacco may cause on biofilms of the human oral microbiome. To do so, we used swabs to sample the oral biofilm of 22 subjects; including 9 control-individuals with no or very low consumption of alcohol and no consumption of tobacco, 7 who were chronic and heavy users of both substances and 6 active smokers that reported no significant alcohol consumption. DNA was extracted from swabs and the V1 region of the 16S rRNA gene was PCR amplified and sequenced using the Ion Torrent PGM platform, generating 3.7 million high quality reads. DNA sequences were clustered and OTUs were assigned using the ARB SILVA database and Qiime . Results We found no differences in species diversity and evenness among the groups. However, we found a significant decrease in species richness in only smokers and in smokers/drinkers when compared to controls. We found that Neisseria abundance was significantly decreased in both groups when compared to controls. Smokers had significant increases in Prevotella and Capnocytophaga and reductions in Granulicatella , Staphylococcus, Peptostreptococcus and Gemella when compared to the two other groups. Controls showed higher abundance of Aggregibacter , whilst smokers/drinkers had lower abundances of Fusobacteria . Samples from only smokers clustered closer together than to controls and smokers/drinkers, and also had a significant reduction in inter-group dissimilarity distances, indicating a more homogenous group than controls. Conclusions Our results indicate that the continued use of tobacco or alcohol plus tobacco significantly reduces bacterial richness, which apparently leads to a reduction in inter-group variability, turning the respective biofilms into a more homogenous microenvironment in terms of bacterial community composition, with possible consequences for human oral diseases.
AbstractList Background Today there are more than 2 billion alcohol users and about 1.3 billion tobacco users worldwide. The chronic and heavy use of these two substances is at the heart of numerous diseases and may wreak havoc on the human oral microbiome. This study delves into the changes that alcohol and tobacco may cause on biofilms of the human oral microbiome. To do so, we used swabs to sample the oral biofilm of 22 subjects; including 9 control-individuals with no or very low consumption of alcohol and no consumption of tobacco, 7 who were chronic and heavy users of both substances and 6 active smokers that reported no significant alcohol consumption. DNA was extracted from swabs and the V1 region of the 16S rRNA gene was PCR amplified and sequenced using the Ion Torrent PGM platform, generating 3.7 million high quality reads. DNA sequences were clustered and OTUs were assigned using the ARB SILVA database and Qiime . Results We found no differences in species diversity and evenness among the groups. However, we found a significant decrease in species richness in only smokers and in smokers/drinkers when compared to controls. We found that Neisseria abundance was significantly decreased in both groups when compared to controls. Smokers had significant increases in Prevotella and Capnocytophaga and reductions in Granulicatella , Staphylococcus, Peptostreptococcus and Gemella when compared to the two other groups. Controls showed higher abundance of Aggregibacter , whilst smokers/drinkers had lower abundances of Fusobacteria . Samples from only smokers clustered closer together than to controls and smokers/drinkers, and also had a significant reduction in inter-group dissimilarity distances, indicating a more homogenous group than controls. Conclusions Our results indicate that the continued use of tobacco or alcohol plus tobacco significantly reduces bacterial richness, which apparently leads to a reduction in inter-group variability, turning the respective biofilms into a more homogenous microenvironment in terms of bacterial community composition, with possible consequences for human oral diseases.
Background: Today there are more than 2 billion alcohol users and about 1.3 billion tobacco users worldwide. The chronic and heavy use of these two substances is at the heart of numerous diseases and may wreak havoc on the human oral microbiome. This study delves into the changes that alcohol and tobacco may cause on biofilms of the human oral microbiome. To do so, we used swabs to sample the oral biofilm of 22 subjects; including 9 control-individuals with no or very low consumption of alcohol and no consumption of tobacco, 7 who were chronic and heavy users of both substances and 6 active smokers that reported no significant alcohol consumption. DNA was extracted from swabs and the V1 region of the 16S rRNA gene was PCR amplified and sequenced using the Ion Torrent PGM platform, generating 3.7 million high quality reads. DNA sequences were clustered and OTUs were assigned using the ARB SILVA database and Qiime. Results: We found no differences in species diversity and evenness among the groups. However, we found a significant decrease in species richness in only smokers and in smokers/drinkers when compared to controls. We found that Neisseria abundance was significantly decreased in both groups when compared to controls. Smokers had significant increases in Prevotella and Capnocytophaga and reductions in Granulicatella, Staphylococcus, Peptostreptococcus and Gemella when compared to the two other groups. Controls showed higher abundance of Aggregibacter, whilst smokers/drinkers had lower abundances of Fusobacteria. Samples from only smokers clustered closer together than to controls and smokers/drinkers, and also had a significant reduction in inter-group dissimilarity distances, indicating a more homogenous group than controls. Conclusions: Our results indicate that the continued use of tobacco or alcohol plus tobacco significantly reduces bacterial richness, which apparently leads to a reduction in inter-group variability, turning the respective biofilms into a more homogenous microenvironment in terms of bacterial community composition, with possible consequences for human oral diseases.
Today there are more than 2 billion alcohol users and about 1.3 billion tobacco users worldwide. The chronic and heavy use of these two substances is at the heart of numerous diseases and may wreak havoc on the human oral microbiome. This study delves into the changes that alcohol and tobacco may cause on biofilms of the human oral microbiome. To do so, we used swabs to sample the oral biofilm of 22 subjects; including 9 control-individuals with no or very low consumption of alcohol and no consumption of tobacco, 7 who were chronic and heavy users of both substances and 6 active smokers that reported no significant alcohol consumption. DNA was extracted from swabs and the V1 region of the 16S rRNA gene was PCR amplified and sequenced using the Ion Torrent PGM platform, generating 3.7 million high quality reads. DNA sequences were clustered and OTUs were assigned using the ARB SILVA database and Qiime.BACKGROUNDToday there are more than 2 billion alcohol users and about 1.3 billion tobacco users worldwide. The chronic and heavy use of these two substances is at the heart of numerous diseases and may wreak havoc on the human oral microbiome. This study delves into the changes that alcohol and tobacco may cause on biofilms of the human oral microbiome. To do so, we used swabs to sample the oral biofilm of 22 subjects; including 9 control-individuals with no or very low consumption of alcohol and no consumption of tobacco, 7 who were chronic and heavy users of both substances and 6 active smokers that reported no significant alcohol consumption. DNA was extracted from swabs and the V1 region of the 16S rRNA gene was PCR amplified and sequenced using the Ion Torrent PGM platform, generating 3.7 million high quality reads. DNA sequences were clustered and OTUs were assigned using the ARB SILVA database and Qiime.We found no differences in species diversity and evenness among the groups. However, we found a significant decrease in species richness in only smokers and in smokers/drinkers when compared to controls. We found that Neisseria abundance was significantly decreased in both groups when compared to controls. Smokers had significant increases in Prevotella and Capnocytophaga and reductions in Granulicatella, Staphylococcus, Peptostreptococcus and Gemella when compared to the two other groups. Controls showed higher abundance of Aggregibacter, whilst smokers/drinkers had lower abundances of Fusobacteria. Samples from only smokers clustered closer together than to controls and smokers/drinkers, and also had a significant reduction in inter-group dissimilarity distances, indicating a more homogenous group than controls.RESULTSWe found no differences in species diversity and evenness among the groups. However, we found a significant decrease in species richness in only smokers and in smokers/drinkers when compared to controls. We found that Neisseria abundance was significantly decreased in both groups when compared to controls. Smokers had significant increases in Prevotella and Capnocytophaga and reductions in Granulicatella, Staphylococcus, Peptostreptococcus and Gemella when compared to the two other groups. Controls showed higher abundance of Aggregibacter, whilst smokers/drinkers had lower abundances of Fusobacteria. Samples from only smokers clustered closer together than to controls and smokers/drinkers, and also had a significant reduction in inter-group dissimilarity distances, indicating a more homogenous group than controls.Our results indicate that the continued use of tobacco or alcohol plus tobacco significantly reduces bacterial richness, which apparently leads to a reduction in inter-group variability, turning the respective biofilms into a more homogenous microenvironment in terms of bacterial community composition, with possible consequences for human oral diseases.CONCLUSIONSOur results indicate that the continued use of tobacco or alcohol plus tobacco significantly reduces bacterial richness, which apparently leads to a reduction in inter-group variability, turning the respective biofilms into a more homogenous microenvironment in terms of bacterial community composition, with possible consequences for human oral diseases.
Today there are more than 2 billion alcohol users and about 1.3 billion tobacco users worldwide. The chronic and heavy use of these two substances is at the heart of numerous diseases and may wreak havoc on the human oral microbiome. This study delves into the changes that alcohol and tobacco may cause on biofilms of the human oral microbiome. To do so, we used swabs to sample the oral biofilm of 22 subjects; including 9 control-individuals with no or very low consumption of alcohol and no consumption of tobacco, 7 who were chronic and heavy users of both substances and 6 active smokers that reported no significant alcohol consumption. DNA was extracted from swabs and the V1 region of the 16S rRNA gene was PCR amplified and sequenced using the Ion Torrent PGM platform, generating 3.7 million high quality reads. DNA sequences were clustered and OTUs were assigned using the ARB SILVA database and Qiime. We found no differences in species diversity and evenness among the groups. However, we found a significant decrease in species richness in only smokers and in smokers/drinkers when compared to controls. We found that Neisseria abundance was significantly decreased in both groups when compared to controls. Smokers had significant increases in Prevotella and Capnocytophaga and reductions in Granulicatella, Staphylococcus, Peptostreptococcus and Gemella when compared to the two other groups. Controls showed higher abundance of Aggregibacter, whilst smokers/drinkers had lower abundances of Fusobacteria. Samples from only smokers clustered closer together than to controls and smokers/drinkers, and also had a significant reduction in inter-group dissimilarity distances, indicating a more homogenous group than controls. Our results indicate that the continued use of tobacco or alcohol plus tobacco significantly reduces bacterial richness, which apparently leads to a reduction in inter-group variability, turning the respective biofilms into a more homogenous microenvironment in terms of bacterial community composition, with possible consequences for human oral diseases.
Doc number: 250 Abstract Background: Today there are more than 2 billion alcohol users and about 1.3 billion tobacco users worldwide. The chronic and heavy use of these two substances is at the heart of numerous diseases and may wreak havoc on the human oral microbiome. This study delves into the changes that alcohol and tobacco may cause on biofilms of the human oral microbiome. To do so, we used swabs to sample the oral biofilm of 22 subjects; including 9 control-individuals with no or very low consumption of alcohol and no consumption of tobacco, 7 who were chronic and heavy users of both substances and 6 active smokers that reported no significant alcohol consumption. DNA was extracted from swabs and the V1 region of the 16S rRNA gene was PCR amplified and sequenced using the Ion Torrent PGM platform, generating 3.7 million high quality reads. DNA sequences were clustered and OTUs were assigned using the ARB SILVA database and Qiime . Results: We found no differences in species diversity and evenness among the groups. However, we found a significant decrease in species richness in only smokers and in smokers/drinkers when compared to controls. We found that Neisseria abundance was significantly decreased in both groups when compared to controls. Smokers had significant increases in Prevotella and Capnocytophaga and reductions in Granulicatella , Staphylococcus, Peptostreptococcus and Gemella when compared to the two other groups. Controls showed higher abundance of Aggregibacter , whilst smokers/drinkers had lower abundances of Fusobacteria . Samples from only smokers clustered closer together than to controls and smokers/drinkers, and also had a significant reduction in inter-group dissimilarity distances, indicating a more homogenous group than controls. Conclusions: Our results indicate that the continued use of tobacco or alcohol plus tobacco significantly reduces bacterial richness, which apparently leads to a reduction in inter-group variability, turning the respective biofilms into a more homogenous microenvironment in terms of bacterial community composition, with possible consequences for human oral diseases.
ArticleNumber 250
Author Amorim, Maria
Kowalski, Luiz Paulo
Francisco, Ana Luisa Noronha
Barbosa, Luisa Fernanda
Fernandes, Gustavo Ribeiro
Nunes, Diana Noronha
Thomas, Andrew Maltez
Gleber-Netto, Frederico Omar
Setubal, João Carlos
Dias-Neto, Emmanuel
Guerra de Andrade, Arthur
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  givenname: Andrew Maltez
  surname: Thomas
  fullname: Thomas, Andrew Maltez
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  givenname: Frederico Omar
  surname: Gleber-Netto
  fullname: Gleber-Netto, Frederico Omar
  organization: Laboratory of Medical Genomics, Centro Internacional de Pesquisa, AC Camargo Cancer Center, Curso de Ps-graduao em Oncologia, Fundao Antnio Prudente/AC Camargo Cancer Center
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  givenname: Gustavo Ribeiro
  surname: Fernandes
  fullname: Fernandes, Gustavo Ribeiro
  organization: Laboratory of Medical Genomics, Centro Internacional de Pesquisa, AC Camargo Cancer Center
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  givenname: Maria
  surname: Amorim
  fullname: Amorim, Maria
  organization: Laboratory of Medical Genomics, Centro Internacional de Pesquisa, AC Camargo Cancer Center, Curso de Ps-graduao em Oncologia, Fundao Antnio Prudente/AC Camargo Cancer Center
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  givenname: Luisa Fernanda
  surname: Barbosa
  fullname: Barbosa, Luisa Fernanda
  organization: Laboratory of Medical Genomics, Centro Internacional de Pesquisa, AC Camargo Cancer Center, Universidad de Los Andes
– sequence: 6
  givenname: Ana Luisa Noronha
  surname: Francisco
  fullname: Francisco, Ana Luisa Noronha
  organization: Department of Head and Neck Surgery and Otorhinolaryngology, AC Camargo Cancer Center and National Institute of Science and Technology in Oncogenomics (INCITO)
– sequence: 7
  givenname: Arthur
  surname: Guerra de Andrade
  fullname: Guerra de Andrade, Arthur
  organization: Department of Psychiatry, Universidade de So Paulo and of Faculdade de Medicina do ABC
– sequence: 8
  givenname: João Carlos
  surname: Setubal
  fullname: Setubal, João Carlos
  organization: Departmento de Bioqumica, Instituto de Qumica, Universidade de So Paulo, Virginia Bioinformatics Institute, Virginia Tech
– sequence: 9
  givenname: Luiz Paulo
  surname: Kowalski
  fullname: Kowalski, Luiz Paulo
  organization: Department of Head and Neck Surgery and Otorhinolaryngology, AC Camargo Cancer Center and National Institute of Science and Technology in Oncogenomics (INCITO)
– sequence: 10
  givenname: Diana Noronha
  surname: Nunes
  fullname: Nunes, Diana Noronha
  organization: Laboratory of Medical Genomics, Centro Internacional de Pesquisa, AC Camargo Cancer Center
– sequence: 11
  givenname: Emmanuel
  surname: Dias-Neto
  fullname: Dias-Neto, Emmanuel
  email: emmanuel@usp.br
  organization: Laboratory of Medical Genomics, Centro Internacional de Pesquisa, AC Camargo Cancer Center, Laboratory of Neurosciences (LIM27), Institute of Psychiatry, Faculdade de Medicina, Universidade de So Paulo
BackLink https://www.ncbi.nlm.nih.gov/pubmed/25278091$$D View this record in MEDLINE/PubMed
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2014 Thomas et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
Thomas et al.; licensee BioMed Central Ltd. 2014
Copyright_xml – notice: Thomas et al.; licensee BioMed Central Ltd. 2014 This article is published under license to BioMed Central Ltd. 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 work is properly credited. The Creative Commons Public Domain Dedication waiver ( ) applies to the data made available in this article, unless otherwise stated.
– notice: 2014 Thomas et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
– notice: Thomas et al.; licensee BioMed Central Ltd. 2014
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Issue 1
Keywords Oral cavity
16S rRNA
Alcohol
Tobacco
Microbiome
Language English
License This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
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Snippet Background Today there are more than 2 billion alcohol users and about 1.3 billion tobacco users worldwide. The chronic and heavy use of these two substances...
Today there are more than 2 billion alcohol users and about 1.3 billion tobacco users worldwide. The chronic and heavy use of these two substances is at the...
Doc number: 250 Abstract Background: Today there are more than 2 billion alcohol users and about 1.3 billion tobacco users worldwide. The chronic and heavy use...
Background: Today there are more than 2 billion alcohol users and about 1.3 billion tobacco users worldwide. The chronic and heavy use of these two substances...
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StartPage 250
SubjectTerms Aged
Alcohol Drinking
Alcohol use
Alcohols
Bacteria - classification
Bacteria - genetics
Bacteria - isolation & purification
Biofilms
Biofilms - growth & development
Biological Microscopy
Biomedical and Life Sciences
Biota - drug effects
Cancer
Capnocytophaga
Cluster Analysis
Community composition
Consumption
Deoxyribonucleic acid
DNA
DNA, Bacterial - chemistry
DNA, Bacterial - genetics
DNA, Ribosomal - chemistry
DNA, Ribosomal - genetics
Ecological and evolutionary microbiology
Female
Gram-positive bacteria
Humans
Laboratories
Life Sciences
Male
Microbiology
Middle Aged
Molecular Sequence Data
Mortality
Mouth Mucosa - microbiology
Mycology
Neisseria
Otolaryngology
Parasitology
Peptostreptococcus
Phylogeny
Polymerase Chain Reaction
Prevotella
Research Article
RNA, Ribosomal, 16S - genetics
Sequence Analysis, DNA
Species diversity
Species richness
Staphylococcus
Tobacco
Tobacco Use
Virology
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Title Alcohol and tobacco consumption affects bacterial richness in oral cavity mucosa biofilms
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