The Role of Bacteria in the Pathogenesis and Progression of Idiopathic Pulmonary Fibrosis
Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease of unknown cause that leads to respiratory failure and death within 5 years of diagnosis. Overt respiratory infection and immunosuppression carry a high morbidity and mortality, and polymorphisms in genes related to epithelial integri...
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| Vydáno v: | American journal of respiratory and critical care medicine Ročník 190; číslo 8; s. 906 - 913 |
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| Hlavní autoři: | , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
United States
American Thoracic Society
15.10.2014
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| Témata: | |
| ISSN: | 1073-449X, 1535-4970, 1535-4970 |
| On-line přístup: | Získat plný text |
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| Abstract | Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease of unknown cause that leads to respiratory failure and death within 5 years of diagnosis. Overt respiratory infection and immunosuppression carry a high morbidity and mortality, and polymorphisms in genes related to epithelial integrity and host defense predispose to IPF.
To investigate the role of bacteria in the pathogenesis and progression of IPF.
We prospectively enrolled patients diagnosed with IPF according to international criteria together with healthy smokers, nonsmokers, and subjects with moderate chronic obstructive pulmonary disease as control subjects. Subjects underwent bronchoalveolar lavage (BAL), from which genomic DNA was isolated. The V3-V5 region of the bacterial 16S rRNA gene was amplified, allowing quantification of bacterial load and identification of communities by 16S rRNA quantitative polymerase chain reaction and pyrosequencing.
Sixty-five patients with IPF had double the burden of bacteria in BAL fluid compared with 44 control subjects. Baseline bacterial burden predicted the rate of decline in lung volume and risk of death and associated independently with the rs35705950 polymorphism of the MUC5B mucin gene, a proven host susceptibility factor for IPF. Sequencing yielded 912,883 high-quality reads from all subjects. We identified Haemophilus, Streptococcus, Neisseria, and Veillonella spp. to be more abundant in cases than control subjects. Regression analyses indicated that these specific operational taxonomic units as well as bacterial burden associated independently with IPF.
IPF is characterized by an increased bacterial burden in BAL that predicts decline in lung function and death. Trials of antimicrobial therapy are needed to determine if microbial burden is pathogenic in the disease. |
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| AbstractList | Rationale: Idiopathic pulmonary fibrosis (IPF) is a progressive lung
disease of unknown cause that leads to respiratory failure and death within 5 years
of diagnosis. Overt respiratory infection and immunosuppression carry a high
morbidity and mortality, and polymorphisms in genes related to epithelial integrity
and host defense predispose to IPF. Objectives: To investigate the role of bacteria in the pathogenesis and
progression of IPF. Methods: We prospectively enrolled patients diagnosed with IPF according
to international criteria together with healthy smokers, nonsmokers, and subjects
with moderate chronic obstructive pulmonary disease as control subjects. Subjects
underwent bronchoalveolar lavage (BAL), from which genomic DNA was isolated. The
V3–V5 region of the bacterial 16S rRNA gene was amplified, allowing
quantification of bacterial load and identification of communities by 16S rRNA
quantitative polymerase chain reaction and pyrosequencing. Measurements and Main Results: Sixty-five patients with IPF had double
the burden of bacteria in BAL fluid compared with 44 control subjects. Baseline
bacterial burden predicted the rate of decline in lung volume and risk of death and
associated independently with the rs35705950 polymorphism of the MUC5B mucin gene, a
proven host susceptibility factor for IPF. Sequencing yielded 912,883 high-quality
reads from all subjects. We identified Haemophilus,
Streptococcus, Neisseria, and
Veillonella spp. to be more abundant in cases than control
subjects. Regression analyses indicated that these specific operational taxonomic
units as well as bacterial burden associated independently with IPF. Conclusions: IPF is characterized by an increased bacterial burden in
BAL that predicts decline in lung function and death. Trials of antimicrobial therapy
are needed to determine if microbial burden is pathogenic in the disease. Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease of unknown cause that leads to respiratory failure and death within 5 years of diagnosis. Overt respiratory infection and immunosuppression carry a high morbidity and mortality, and polymorphisms in genes related to epithelial integrity and host defense predispose to IPF.RATIONALEIdiopathic pulmonary fibrosis (IPF) is a progressive lung disease of unknown cause that leads to respiratory failure and death within 5 years of diagnosis. Overt respiratory infection and immunosuppression carry a high morbidity and mortality, and polymorphisms in genes related to epithelial integrity and host defense predispose to IPF.To investigate the role of bacteria in the pathogenesis and progression of IPF.OBJECTIVESTo investigate the role of bacteria in the pathogenesis and progression of IPF.We prospectively enrolled patients diagnosed with IPF according to international criteria together with healthy smokers, nonsmokers, and subjects with moderate chronic obstructive pulmonary disease as control subjects. Subjects underwent bronchoalveolar lavage (BAL), from which genomic DNA was isolated. The V3-V5 region of the bacterial 16S rRNA gene was amplified, allowing quantification of bacterial load and identification of communities by 16S rRNA quantitative polymerase chain reaction and pyrosequencing.METHODSWe prospectively enrolled patients diagnosed with IPF according to international criteria together with healthy smokers, nonsmokers, and subjects with moderate chronic obstructive pulmonary disease as control subjects. Subjects underwent bronchoalveolar lavage (BAL), from which genomic DNA was isolated. The V3-V5 region of the bacterial 16S rRNA gene was amplified, allowing quantification of bacterial load and identification of communities by 16S rRNA quantitative polymerase chain reaction and pyrosequencing.Sixty-five patients with IPF had double the burden of bacteria in BAL fluid compared with 44 control subjects. Baseline bacterial burden predicted the rate of decline in lung volume and risk of death and associated independently with the rs35705950 polymorphism of the MUC5B mucin gene, a proven host susceptibility factor for IPF. Sequencing yielded 912,883 high-quality reads from all subjects. We identified Haemophilus, Streptococcus, Neisseria, and Veillonella spp. to be more abundant in cases than control subjects. Regression analyses indicated that these specific operational taxonomic units as well as bacterial burden associated independently with IPF.MEASUREMENTS AND MAIN RESULTSSixty-five patients with IPF had double the burden of bacteria in BAL fluid compared with 44 control subjects. Baseline bacterial burden predicted the rate of decline in lung volume and risk of death and associated independently with the rs35705950 polymorphism of the MUC5B mucin gene, a proven host susceptibility factor for IPF. Sequencing yielded 912,883 high-quality reads from all subjects. We identified Haemophilus, Streptococcus, Neisseria, and Veillonella spp. to be more abundant in cases than control subjects. Regression analyses indicated that these specific operational taxonomic units as well as bacterial burden associated independently with IPF.IPF is characterized by an increased bacterial burden in BAL that predicts decline in lung function and death. Trials of antimicrobial therapy are needed to determine if microbial burden is pathogenic in the disease.CONCLUSIONSIPF is characterized by an increased bacterial burden in BAL that predicts decline in lung function and death. Trials of antimicrobial therapy are needed to determine if microbial burden is pathogenic in the disease. Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease of unknown cause that leads to respiratory failure and death within 5 years of diagnosis. Overt respiratory infection and immunosuppression carry a high morbidity and mortality, and polymorphisms in genes related to epithelial integrity and host defense predispose to IPF. To investigate the role of bacteria in the pathogenesis and progression of IPF. We prospectively enrolled patients diagnosed with IPF according to international criteria together with healthy smokers, nonsmokers, and subjects with moderate chronic obstructive pulmonary disease as control subjects. Subjects underwent bronchoalveolar lavage (BAL), from which genomic DNA was isolated. The V3-V5 region of the bacterial 16S rRNA gene was amplified, allowing quantification of bacterial load and identification of communities by 16S rRNA quantitative polymerase chain reaction and pyrosequencing. Sixty-five patients with IPF had double the burden of bacteria in BAL fluid compared with 44 control subjects. Baseline bacterial burden predicted the rate of decline in lung volume and risk of death and associated independently with the rs35705950 polymorphism of the MUC5B mucin gene, a proven host susceptibility factor for IPF. Sequencing yielded 912,883 high-quality reads from all subjects. We identified Haemophilus, Streptococcus, Neisseria, and Veillonella spp. to be more abundant in cases than control subjects. Regression analyses indicated that these specific operational taxonomic units as well as bacterial burden associated independently with IPF. IPF is characterized by an increased bacterial burden in BAL that predicts decline in lung function and death. Trials of antimicrobial therapy are needed to determine if microbial burden is pathogenic in the disease. Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease of unknown cause that leads to respiratory failure and death within 5 years of diagnosis. Overt respiratory infection and immunosuppression carry a high morbidity and mortality, and polymorphisms in genes related to epithelial integrity and host defense predispose to IPF. To investigate the role of bacteria in the pathogenesis and progression of IPF. We prospectively enrolled patients diagnosed with IPF according to international criteria together with healthy smokers, nonsmokers, and subjects with moderate chronic obstructive pulmonary disease as control subjects. Subjects underwent bronchoalveolar lavage (BAL), from which genomic DNA was isolated. The V3-V5 region of the bacterial 16S rRNA gene was amplified, allowing quantification of bacterial load and identification of communities by 16S rRNA quantitative polymerase chain reaction and pyrosequencing. Sixty-five patients with IPF had double the burden of bacteria in BAL fluid compared with 44 control subjects. Baseline bacterial burden predicted the rate of decline in lung volume and risk of death and associated independently with the rs35705950 polymorphism of the MUC5B mucin gene, a proven host susceptibility factor for IPF. Sequencing yielded 912,883 high-quality reads from all subjects. We identified Haemophilus, Streptococcus, Neisseria, and Veillonella spp. to be more abundant in cases than control subjects. Regression analyses indicated that these specific operational taxonomic units as well as bacterial burden associated independently with IPF. IPF is characterized by an increased bacterial burden in BAL that predicts decline in lung function and death. Trials of antimicrobial therapy are needed to determine if microbial burden is pathogenic in the disease. |
| Author | Russell, Kirsty E. Cookson, William O. C. Schwartz, David A. Willis-Owen, Saffron A. G. Molyneaux, Phillip L. Murphy, Elissa Cox, Michael J. Russell, Anne-Marie Moffatt, Miriam F. Maher, Toby M. Johnston, Sebastian L. Wells, Athol U. Mallia, Patrick |
| Author_xml | – sequence: 1 givenname: Phillip L. surname: Molyneaux fullname: Molyneaux, Phillip L. organization: National Heart and Lung Institute, Imperial College, London, United Kingdom, National Institute for Health Research Respiratory Biomedical Research Unit, Royal Brompton Hospital, London, United Kingdom – sequence: 2 givenname: Michael J. surname: Cox fullname: Cox, Michael J. organization: National Heart and Lung Institute, Imperial College, London, United Kingdom – sequence: 3 givenname: Saffron A. G. surname: Willis-Owen fullname: Willis-Owen, Saffron A. G. organization: National Heart and Lung Institute, Imperial College, London, United Kingdom – sequence: 4 givenname: Patrick surname: Mallia fullname: Mallia, Patrick organization: National Heart and Lung Institute, Imperial College, London, United Kingdom, Imperial College Healthcare National Health Service Trust, London, United Kingdom; and – sequence: 5 givenname: Kirsty E. surname: Russell fullname: Russell, Kirsty E. organization: National Heart and Lung Institute, Imperial College, London, United Kingdom – sequence: 6 givenname: Anne-Marie surname: Russell fullname: Russell, Anne-Marie organization: National Heart and Lung Institute, Imperial College, London, United Kingdom, National Institute for Health Research Respiratory Biomedical Research Unit, Royal Brompton Hospital, London, United Kingdom – sequence: 7 givenname: Elissa surname: Murphy fullname: Murphy, Elissa organization: Department of Medicine, University of Colorado, Denver, Colorado – sequence: 8 givenname: Sebastian L. surname: Johnston fullname: Johnston, Sebastian L. organization: National Heart and Lung Institute, Imperial College, London, United Kingdom, Imperial College Healthcare National Health Service Trust, London, United Kingdom; and – sequence: 9 givenname: David A. surname: Schwartz fullname: Schwartz, David A. organization: Department of Medicine, University of Colorado, Denver, Colorado – sequence: 10 givenname: Athol U. surname: Wells fullname: Wells, Athol U. organization: National Institute for Health Research Respiratory Biomedical Research Unit, Royal Brompton Hospital, London, United Kingdom – sequence: 11 givenname: William O. C. surname: Cookson fullname: Cookson, William O. C. organization: National Heart and Lung Institute, Imperial College, London, United Kingdom, National Institute for Health Research Respiratory Biomedical Research Unit, Royal Brompton Hospital, London, United Kingdom – sequence: 12 givenname: Toby M. surname: Maher fullname: Maher, Toby M. organization: National Heart and Lung Institute, Imperial College, London, United Kingdom, National Institute for Health Research Respiratory Biomedical Research Unit, Royal Brompton Hospital, London, United Kingdom – sequence: 13 givenname: Miriam F. surname: Moffatt fullname: Moffatt, Miriam F. organization: National Heart and Lung Institute, Imperial College, London, United Kingdom |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25184687$$D View this record in MEDLINE/PubMed |
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| Snippet | Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease of unknown cause that leads to respiratory failure and death within 5 years of diagnosis.... Rationale: Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease of unknown cause that leads to respiratory failure and death within 5 years of... |
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| SubjectTerms | Aged Bacteria Bacteria - isolation & purification Bacterial Load Bronchoalveolar Lavage Bronchoalveolar Lavage Fluid - microbiology Bronchoscopy Case-Control Studies Chronic obstructive pulmonary disease Disease Progression DNA, Bacterial - analysis Female Genes Genetic Markers Genotyping Techniques Humans Idiopathic Pulmonary Fibrosis - genetics Idiopathic Pulmonary Fibrosis - microbiology Idiopathic Pulmonary Fibrosis - mortality Idiopathic Pulmonary Fibrosis - physiopathology Infections Lavage Logistic Models Lung diseases Male Microbiota Middle Aged Mortality Mucin-5B - genetics Original Pathogenesis Polymerase Chain Reaction Polymorphism Polymorphism, Genetic Prospective Studies Pulmonary fibrosis Sequence Analysis, DNA Taxonomy |
| Title | The Role of Bacteria in the Pathogenesis and Progression of Idiopathic Pulmonary Fibrosis |
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