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Lung microbiome and origins of the respiratory diseases
The studies on the composition of the human microbiomes in healthy individuals, its variability in the course of inflammation, infection, antibiotic therapy, diets and different pathological conditions have revealed their intra and inter-kingdom relationships. The lung microbiome comprises of major...
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Published in: | Current research in immunology 2023-01, Vol.4, p.100065-100065, Article 100065 |
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description | The studies on the composition of the human microbiomes in healthy individuals, its variability in the course of inflammation, infection, antibiotic therapy, diets and different pathological conditions have revealed their intra and inter-kingdom relationships. The lung microbiome comprises of major species members of the phylum Bacteroidetes, Firmicutes, Actinobacteria, Fusobacteria and Proteobacteria, which are distributed in ecological niches along nasal cavity, nasopharynx, oropharynx, trachea and in the lungs. Commensal and pathogenic species are maintained in equilibrium as they have strong relationships. Bacterial overgrowth after dysbiosis and/or imbalanced of CD4+ helper T cells, CD8+ cytotoxic T cells and regulatory T cells (Treg) populations can promote lung inflammatory reactions and distress, and consequently acute and chronic respiratory diseases. This review is aimed to summarize the latest advances in resident lung microbiome and its participation in most common pulmonary infections and pneumonia, community-acquired pneumonia (CAP), ventilator-associated pneumonia (VAP), immunodeficiency associated pneumonia, SARS-CoV-2-associated pneumonia, acute respiratory distress syndrome (ARDS) and chronic obstructive pulmonary disease (COPD). We briefly describe physiological and immunological mechanisms that selectively create advantages or disadvantages for relative growth of pathogenic bacterial species in the respiratory tract. At the end, we propose some directions and analytical methods that may facilitate the identification of key genera and species of resident and transient microbes involved in the respiratory diseases’ initiation and progression.
[Display omitted]
•Which is the most reliable method(s) to assess respiratory tract microbiome: oral swabs, pharyngeal secretions, sputum, endotracheal aspirate (ETA), bronchoalveolar lavage fluid (BAL), microlavage (mBAL), bronchoscopy aspiration, plasma samples?•How does one define the normal respiratory tract microbiome, with quantitative and qualitative cut-off points for dysbiosis? Is the approach defended by some investigators acceptable, in the sense that dysbiosis coincides with low alpha and beta diversity and less abundance of “protective” oral-origin commensal bacteria? Which limits should be considered?•Specifically for pneumonia (community acquired, nosocomial and other variants), pathogen cut-off points are essential, as standard microbiome sequencing might elicit many potential agents |
doi_str_mv | 10.1016/j.crimmu.2023.100065 |
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[Display omitted]
•Which is the most reliable method(s) to assess respiratory tract microbiome: oral swabs, pharyngeal secretions, sputum, endotracheal aspirate (ETA), bronchoalveolar lavage fluid (BAL), microlavage (mBAL), bronchoscopy aspiration, plasma samples?•How does one define the normal respiratory tract microbiome, with quantitative and qualitative cut-off points for dysbiosis? Is the approach defended by some investigators acceptable, in the sense that dysbiosis coincides with low alpha and beta diversity and less abundance of “protective” oral-origin commensal bacteria? Which limits should be considered?•Specifically for pneumonia (community acquired, nosocomial and other variants), pathogen cut-off points are essential, as standard microbiome sequencing might elicit many potential agents not necessarily involved in lung disease. Does over 50% relative abundance or a massive pathogen burden as anticipated by some implicate an etiological role?•Is a sharper distinction between the respiratory microbiomes possible, in such diseases as acute respiratory distress syndrome, community acquired pneumonia, ventilator associated pneumonia, and pneumonia in immunodeficient populations?•What are the impact of antibiotics or steroids on bacterial and fungal composition and richness of microbiome? What are airway microbiomes that predispose to a disease and then to recurrent exacerbations?•Novel efficacious mucosal vaccines to respiratory viruses, including respiratory syncytial virus, coronaviruses, paramyxoviruses, rhinoviruses and respiratory enteroviruses might be the best solution to prevent both the upper and lower respiratory tract diseases.</description><identifier>ISSN: 2590-2555</identifier><identifier>EISSN: 2590-2555</identifier><identifier>DOI: 10.1016/j.crimmu.2023.100065</identifier><identifier>PMID: 37456520</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>ARDS ; Community-acquired pneumonia ; COPD ; from the special issue: Role of host-microbiome interactions during pneumonia, edited by Antoine Roquilly and Karim Asehnoune ; Inflammation ; Microbiomes ; Respiratory diseases</subject><ispartof>Current research in immunology, 2023-01, Vol.4, p.100065-100065, Article 100065</ispartof><rights>2023</rights><rights>2023 Published by Elsevier B.V.</rights><rights>2023 Published by Elsevier B.V. 2023</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4455-182fd8e2a982b0b4f00a4f94739026d55145dee3b7d150c1814432a83aa5027f3</citedby><cites>FETCH-LOGICAL-c4455-182fd8e2a982b0b4f00a4f94739026d55145dee3b7d150c1814432a83aa5027f3</cites><orcidid>0000-0002-3832-5279</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10339129/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S2590255523000112$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,3536,27901,27902,45756,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37456520$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Belizário, José</creatorcontrib><creatorcontrib>Garay-Malpartida, Miguel</creatorcontrib><creatorcontrib>Faintuch, Joel</creatorcontrib><title>Lung microbiome and origins of the respiratory diseases</title><title>Current research in immunology</title><addtitle>Curr Res Immunol</addtitle><description>The studies on the composition of the human microbiomes in healthy individuals, its variability in the course of inflammation, infection, antibiotic therapy, diets and different pathological conditions have revealed their intra and inter-kingdom relationships. The lung microbiome comprises of major species members of the phylum Bacteroidetes, Firmicutes, Actinobacteria, Fusobacteria and Proteobacteria, which are distributed in ecological niches along nasal cavity, nasopharynx, oropharynx, trachea and in the lungs. Commensal and pathogenic species are maintained in equilibrium as they have strong relationships. Bacterial overgrowth after dysbiosis and/or imbalanced of CD4+ helper T cells, CD8+ cytotoxic T cells and regulatory T cells (Treg) populations can promote lung inflammatory reactions and distress, and consequently acute and chronic respiratory diseases. This review is aimed to summarize the latest advances in resident lung microbiome and its participation in most common pulmonary infections and pneumonia, community-acquired pneumonia (CAP), ventilator-associated pneumonia (VAP), immunodeficiency associated pneumonia, SARS-CoV-2-associated pneumonia, acute respiratory distress syndrome (ARDS) and chronic obstructive pulmonary disease (COPD). We briefly describe physiological and immunological mechanisms that selectively create advantages or disadvantages for relative growth of pathogenic bacterial species in the respiratory tract. At the end, we propose some directions and analytical methods that may facilitate the identification of key genera and species of resident and transient microbes involved in the respiratory diseases’ initiation and progression.
[Display omitted]
•Which is the most reliable method(s) to assess respiratory tract microbiome: oral swabs, pharyngeal secretions, sputum, endotracheal aspirate (ETA), bronchoalveolar lavage fluid (BAL), microlavage (mBAL), bronchoscopy aspiration, plasma samples?•How does one define the normal respiratory tract microbiome, with quantitative and qualitative cut-off points for dysbiosis? Is the approach defended by some investigators acceptable, in the sense that dysbiosis coincides with low alpha and beta diversity and less abundance of “protective” oral-origin commensal bacteria? Which limits should be considered?•Specifically for pneumonia (community acquired, nosocomial and other variants), pathogen cut-off points are essential, as standard microbiome sequencing might elicit many potential agents not necessarily involved in lung disease. Does over 50% relative abundance or a massive pathogen burden as anticipated by some implicate an etiological role?•Is a sharper distinction between the respiratory microbiomes possible, in such diseases as acute respiratory distress syndrome, community acquired pneumonia, ventilator associated pneumonia, and pneumonia in immunodeficient populations?•What are the impact of antibiotics or steroids on bacterial and fungal composition and richness of microbiome? What are airway microbiomes that predispose to a disease and then to recurrent exacerbations?•Novel efficacious mucosal vaccines to respiratory viruses, including respiratory syncytial virus, coronaviruses, paramyxoviruses, rhinoviruses and respiratory enteroviruses might be the best solution to prevent both the upper and lower respiratory tract diseases.</description><subject>ARDS</subject><subject>Community-acquired pneumonia</subject><subject>COPD</subject><subject>from the special issue: Role of host-microbiome interactions during pneumonia, edited by Antoine Roquilly and Karim Asehnoune</subject><subject>Inflammation</subject><subject>Microbiomes</subject><subject>Respiratory diseases</subject><issn>2590-2555</issn><issn>2590-2555</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>DOA</sourceid><recordid>eNp9kUtP3DAUha2qqCDgH1RVlt3M4HfiTasKlYc0EhtYW35cDx4l8dROkPj3NQQQbFjZuj73u9fnIPSd4DXBRJ7t1i7HYZjXFFNWSxhL8QUdUaHwigohvr67H6LTUnZVQlvFsZTf0CFruZCC4iPUbuZx2wzR5WRjGqAxo29Sjts4liaFZrqHJkPZx2ymlB8bHwuYAuUEHQTTFzh9OY_R3cXf2_Or1ebm8vr8z2blOBdiRToafAfUqI5abHnA2PCgeMsUptILQbjwAMy2ngjsSEc4Z9R0zBhR9w3sGF0vXJ_MTu_rp01-1MlE_VxIeatNnqLrQZPAJRBHfVCKO97aVmHuvGXWBetaU1m_F9Z-tgN4B-OUTf8B-vFljPd6mx40wYwpQlUl_Hwh5PRvhjLpIRYHfW9GSHPRtGOd5JJ2uEr5Iq3OlpIhvM0hWD9lqHd6yVA_ZaiXDGvbj_c7vjW9JlYFvxYBVNcfImRdXITRgY8Z3FRtiZ9P-A8dpa50</recordid><startdate>20230101</startdate><enddate>20230101</enddate><creator>Belizário, José</creator><creator>Garay-Malpartida, Miguel</creator><creator>Faintuch, Joel</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>6I.</scope><scope>AAFTH</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-3832-5279</orcidid></search><sort><creationdate>20230101</creationdate><title>Lung microbiome and origins of the respiratory diseases</title><author>Belizário, José ; Garay-Malpartida, Miguel ; Faintuch, Joel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4455-182fd8e2a982b0b4f00a4f94739026d55145dee3b7d150c1814432a83aa5027f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>ARDS</topic><topic>Community-acquired pneumonia</topic><topic>COPD</topic><topic>from the special issue: Role of host-microbiome interactions during pneumonia, edited by Antoine Roquilly and Karim Asehnoune</topic><topic>Inflammation</topic><topic>Microbiomes</topic><topic>Respiratory diseases</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Belizário, José</creatorcontrib><creatorcontrib>Garay-Malpartida, Miguel</creatorcontrib><creatorcontrib>Faintuch, Joel</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Current research in immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Belizário, José</au><au>Garay-Malpartida, Miguel</au><au>Faintuch, Joel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lung microbiome and origins of the respiratory diseases</atitle><jtitle>Current research in immunology</jtitle><addtitle>Curr Res Immunol</addtitle><date>2023-01-01</date><risdate>2023</risdate><volume>4</volume><spage>100065</spage><epage>100065</epage><pages>100065-100065</pages><artnum>100065</artnum><issn>2590-2555</issn><eissn>2590-2555</eissn><abstract>The studies on the composition of the human microbiomes in healthy individuals, its variability in the course of inflammation, infection, antibiotic therapy, diets and different pathological conditions have revealed their intra and inter-kingdom relationships. The lung microbiome comprises of major species members of the phylum Bacteroidetes, Firmicutes, Actinobacteria, Fusobacteria and Proteobacteria, which are distributed in ecological niches along nasal cavity, nasopharynx, oropharynx, trachea and in the lungs. Commensal and pathogenic species are maintained in equilibrium as they have strong relationships. Bacterial overgrowth after dysbiosis and/or imbalanced of CD4+ helper T cells, CD8+ cytotoxic T cells and regulatory T cells (Treg) populations can promote lung inflammatory reactions and distress, and consequently acute and chronic respiratory diseases. This review is aimed to summarize the latest advances in resident lung microbiome and its participation in most common pulmonary infections and pneumonia, community-acquired pneumonia (CAP), ventilator-associated pneumonia (VAP), immunodeficiency associated pneumonia, SARS-CoV-2-associated pneumonia, acute respiratory distress syndrome (ARDS) and chronic obstructive pulmonary disease (COPD). We briefly describe physiological and immunological mechanisms that selectively create advantages or disadvantages for relative growth of pathogenic bacterial species in the respiratory tract. At the end, we propose some directions and analytical methods that may facilitate the identification of key genera and species of resident and transient microbes involved in the respiratory diseases’ initiation and progression.
[Display omitted]
•Which is the most reliable method(s) to assess respiratory tract microbiome: oral swabs, pharyngeal secretions, sputum, endotracheal aspirate (ETA), bronchoalveolar lavage fluid (BAL), microlavage (mBAL), bronchoscopy aspiration, plasma samples?•How does one define the normal respiratory tract microbiome, with quantitative and qualitative cut-off points for dysbiosis? Is the approach defended by some investigators acceptable, in the sense that dysbiosis coincides with low alpha and beta diversity and less abundance of “protective” oral-origin commensal bacteria? Which limits should be considered?•Specifically for pneumonia (community acquired, nosocomial and other variants), pathogen cut-off points are essential, as standard microbiome sequencing might elicit many potential agents not necessarily involved in lung disease. Does over 50% relative abundance or a massive pathogen burden as anticipated by some implicate an etiological role?•Is a sharper distinction between the respiratory microbiomes possible, in such diseases as acute respiratory distress syndrome, community acquired pneumonia, ventilator associated pneumonia, and pneumonia in immunodeficient populations?•What are the impact of antibiotics or steroids on bacterial and fungal composition and richness of microbiome? What are airway microbiomes that predispose to a disease and then to recurrent exacerbations?•Novel efficacious mucosal vaccines to respiratory viruses, including respiratory syncytial virus, coronaviruses, paramyxoviruses, rhinoviruses and respiratory enteroviruses might be the best solution to prevent both the upper and lower respiratory tract diseases.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>37456520</pmid><doi>10.1016/j.crimmu.2023.100065</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-3832-5279</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | ARDS Community-acquired pneumonia COPD from the special issue: Role of host-microbiome interactions during pneumonia, edited by Antoine Roquilly and Karim Asehnoune Inflammation Microbiomes Respiratory diseases |
title | Lung microbiome and origins of the respiratory diseases |
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