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Article ; Online: Th17 cells in autoimmune demyelinating disease.

Segal, Benjamin Matthew

2010 Volume 32, Issue 1, Page(s) 71–77

Abstract: Recently published studies in multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE) have demonstrated an association between the development of demyelinating plaques and the accumulation of Th17 cells in the central nervous system ... ...

Abstract	Recently published studies in multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE) have demonstrated an association between the development of demyelinating plaques and the accumulation of Th17 cells in the central nervous system and periphery. However, a causal relationship has been difficult to establish. In fact, in reports published thus far, interleukin (IL)-17A deficiency or neutralization in vivo attenuates, but does not completely abrogate, EAE. There is growing evidence that clinically similar forms of autoimmune demyelinating disease can be driven by myelin-specific T cells of distinct lineages with different degrees of dependence on IL-17A production to achieve their pathological effects. While such observations cast doubts about the potential therapeutic efficacy of Th17 blocking agents in MS, the collective data suggest that IL-17A expression in peripheral blood mononuclear cells could serve as a surrogate biomarker of neuroinflammation and plaque formation and be a useful outcome measure for future clinical trials.
MeSH term(s)	Animals ; Autoimmunity/immunology ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Encephalomyelitis, Autoimmune, Experimental/pathology ; Humans ; Interleukin-17/immunology ; Multiple Sclerosis/immunology ; Multiple Sclerosis/pathology ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes, Helper-Inducer/immunology
Chemical Substances	Interleukin-17
Language	English
Publishing date	2010-02-27
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2316828-6
ISSN	1863-2300 ; 1863-2297
ISSN (online)	1863-2300
ISSN	1863-2297
DOI	10.1007/s00281-009-0186-z
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Article ; Online: Pleural fluid microbiota as a biomarker for malignancy and prognosis.

Kwok, Benjamin / Wu, Benjamin G / Kocak, Ibrahim F / Sulaiman, Imran / Schluger, Rosemary / Li, Yonghua / Anwer, Raheel / Goparaju, Chandra / Ryan, Daniel J / Sagatelian, Marla / Dreier, Matthew S / Murthy, Vivek / Rafeq, Samaan / Michaud, Gaetane C / Sterman, Daniel H / Bessich, Jamie L / Pass, Harvey I / Segal, Leopoldo N / Tsay, Jun-Chieh J

Scientific reports

2023 Volume 13, Issue 1, Page(s) 2229

Abstract: Malignant pleural effusions (MPE) complicate malignancies and portend worse outcomes. MPE is comprised of various components, including immune cells, cancer cells, and cell-free DNA/RNA. There have been investigations into using these components to ... ...

Abstract	Malignant pleural effusions (MPE) complicate malignancies and portend worse outcomes. MPE is comprised of various components, including immune cells, cancer cells, and cell-free DNA/RNA. There have been investigations into using these components to diagnose and prognosticate MPE. We hypothesize that the microbiome of MPE is unique and may be associated with diagnosis and prognosis. We compared the microbiota of MPE against microbiota of pleural effusions from non-malignant and paramalignant states. We collected a total of 165 pleural fluid samples from 165 subjects; Benign (n = 16), Paramalignant (n = 21), MPE-Lung (n = 57), MPE-Other (n = 22), and Mesothelioma (n = 49). We performed high throughput 16S rRNA gene sequencing on pleural fluid samples and controls. We showed that there are compositional differences among pleural effusions related to non-malignant, paramalignant, and malignant disease. Furthermore, we showed differential enrichment of bacterial taxa within MPE depending on the site of primary malignancy. Pleural fluid of MPE-Lung and Mesothelioma were associated with enrichment with oral and gut bacteria that are commonly thought to be commensals, including Rickettsiella, Ruminococcus, Enterococcus, and Lactobacillales. Mortality in MPE-Lung is associated with enrichment in Methylobacterium, Blattabacterium, and Deinococcus. These observations lay the groundwork for future studies that explore host-microbiome interactions and their influence on carcinogenesis.
MeSH term(s)	Humans ; RNA, Ribosomal, 16S/genetics ; Pleural Effusion, Malignant/diagnosis ; Mesothelioma/diagnosis ; Mesothelioma/pathology ; Biomarkers ; Pleural Effusion/diagnosis ; Mesothelioma, Malignant ; Prognosis ; Microbiota/genetics ; Lung Neoplasms/diagnosis ; Lung Neoplasms/complications
Chemical Substances	RNA, Ribosomal, 16S ; Biomarkers
Language	English
Publishing date	2023-02-08
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-29001-4
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Article ; Online: Pleural fluid microbiota as a biomarker for malignancy and prognosis

Benjamin Kwok / Benjamin G. Wu / Ibrahim F. Kocak / Imran Sulaiman / Rosemary Schluger / Yonghua Li / Raheel Anwer / Chandra Goparaju / Daniel J. Ryan / Marla Sagatelian / Matthew S. Dreier / Vivek Murthy / Samaan Rafeq / Gaetane C. Michaud / Daniel H. Sterman / Jamie L. Bessich / Harvey I. Pass / Leopoldo N. Segal / Jun-Chieh J. Tsay

Scientific Reports, Vol 13, Iss 1, Pp 1-

2023 Volume 11

Abstract: Abstract Malignant pleural effusions (MPE) complicate malignancies and portend worse outcomes. MPE is comprised of various components, including immune cells, cancer cells, and cell-free DNA/RNA. There have been investigations into using these components ...

Abstract	Abstract Malignant pleural effusions (MPE) complicate malignancies and portend worse outcomes. MPE is comprised of various components, including immune cells, cancer cells, and cell-free DNA/RNA. There have been investigations into using these components to diagnose and prognosticate MPE. We hypothesize that the microbiome of MPE is unique and may be associated with diagnosis and prognosis. We compared the microbiota of MPE against microbiota of pleural effusions from non-malignant and paramalignant states. We collected a total of 165 pleural fluid samples from 165 subjects; Benign (n = 16), Paramalignant (n = 21), MPE-Lung (n = 57), MPE-Other (n = 22), and Mesothelioma (n = 49). We performed high throughput 16S rRNA gene sequencing on pleural fluid samples and controls. We showed that there are compositional differences among pleural effusions related to non-malignant, paramalignant, and malignant disease. Furthermore, we showed differential enrichment of bacterial taxa within MPE depending on the site of primary malignancy. Pleural fluid of MPE-Lung and Mesothelioma were associated with enrichment with oral and gut bacteria that are commonly thought to be commensals, including Rickettsiella, Ruminococcus, Enterococcus, and Lactobacillales. Mortality in MPE-Lung is associated with enrichment in Methylobacterium, Blattabacterium, and Deinococcus. These observations lay the groundwork for future studies that explore host-microbiome interactions and their influence on carcinogenesis.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2023-02-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
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Article ; Online: Lower Airway Dysbiosis Augments Lung Inflammatory Injury in Mild-to-Moderate Chronic Obstructive Pulmonary Disease.

Sulaiman, Imran / Wu, Benjamin G / Chung, Matthew / Isaacs, Bradley / Tsay, Jun-Chieh J / Holub, Meredith / Barnett, Clea R / Kwok, Benjamin / Kugler, Matthias C / Natalini, Jake G / Singh, Shivani / Li, Yonghua / Schluger, Rosemary / Carpenito, Joseph / Collazo, Destiny / Perez, Luisanny / Kyeremateng, Yaa / Chang, Miao / Campbell, Christina D /

Hansbro, Philip M / Oppenheimer, Beno W / Berger, Kenneth I / Goldring, Roberta M / Koralov, Sergei B / Weiden, Michael D / Xiao, Rui / D'Armiento, Jeanine / Clemente, Jose C / Ghedin, Elodie / Segal, Leopoldo N

American journal of respiratory and critical care medicine

2023 Volume 208, Issue 10, Page(s) 1101–1114

Abstract: Rationale: ...

Abstract	Rationale:
MeSH term(s)	Humans ; Animals ; Mice ; Dysbiosis/complications ; RNA, Ribosomal, 16S ; Pulmonary Disease, Chronic Obstructive/genetics ; Inflammation/complications ; Lung Injury/complications ; Lung/pathology
Chemical Substances	RNA, Ribosomal, 16S
Language	English
Publishing date	2023-09-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1180953-x
ISSN	1535-4970 ; 0003-0805 ; 1073-449X
ISSN (online)	1535-4970
ISSN	0003-0805 ; 1073-449X
DOI	10.1164/rccm.202210-1865OC
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Article ; Online: CRAF dimerization with ARAF regulates KRAS-driven tumor growth.

Cell reports

2022 Volume 38, Issue 6, Page(s) 110351

Abstract: KRAS, which is mutated in ∼30% of all cancers, activates the RAF-MEK-ERK signaling cascade. CRAF is required for growth of KRAS mutant lung tumors, but the requirement for CRAF kinase activity is unknown. Here, we show that subsets of KRAS mutant tumors ... ...

Abstract	KRAS, which is mutated in ∼30% of all cancers, activates the RAF-MEK-ERK signaling cascade. CRAF is required for growth of KRAS mutant lung tumors, but the requirement for CRAF kinase activity is unknown. Here, we show that subsets of KRAS mutant tumors are dependent on CRAF for growth. Kinase-dead but not dimer-defective CRAF rescues growth inhibition, suggesting that dimerization but not kinase activity is required. Quantitative proteomics demonstrates increased levels of CRAF:ARAF dimers in KRAS mutant cells, and depletion of both CRAF and ARAF rescues the CRAF-loss phenotype. Mechanistically, CRAF depletion causes sustained ERK activation and induction of cell-cycle arrest, while treatment with low-dose MEK or ERK inhibitor rescues the CRAF-loss phenotype. Our studies highlight the role of CRAF in regulating MAPK signal intensity to promote tumorigenesis downstream of mutant KRAS and suggest that disrupting CRAF dimerization or degrading CRAF may have therapeutic benefit.
MeSH term(s)	Animals ; Carcinogenesis/drug effects ; Carcinogenesis/metabolism ; Cell Line, Tumor ; Dimerization ; Humans ; MAP Kinase Signaling System/drug effects ; Mice ; Phosphorylation/physiology ; Protein Kinase Inhibitors/pharmacology ; Proto-Oncogene Proteins B-raf/genetics ; Proto-Oncogene Proteins p21(ras)/metabolism ; Signal Transduction/drug effects ; Signal Transduction/physiology ; ras Proteins/genetics
Chemical Substances	KRAS protein, human ; Protein Kinase Inhibitors ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; ras Proteins (EC 3.6.5.2)
Language	English
Publishing date	2022-02-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2022.110351
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Article ; Online: CRAF dimerization with ARAF regulates KRAS-driven tumor growth

Cell Reports, Vol 38, Iss 6, Pp 110351- (2022)

2022

Abstract: Summary: KRAS, which is mutated in ∼30% of all cancers, activates the RAF-MEK-ERK signaling cascade. CRAF is required for growth of KRAS mutant lung tumors, but the requirement for CRAF kinase activity is unknown. Here, we show that subsets of KRAS ... ...

Abstract	Summary: KRAS, which is mutated in ∼30% of all cancers, activates the RAF-MEK-ERK signaling cascade. CRAF is required for growth of KRAS mutant lung tumors, but the requirement for CRAF kinase activity is unknown. Here, we show that subsets of KRAS mutant tumors are dependent on CRAF for growth. Kinase-dead but not dimer-defective CRAF rescues growth inhibition, suggesting that dimerization but not kinase activity is required. Quantitative proteomics demonstrates increased levels of CRAF:ARAF dimers in KRAS mutant cells, and depletion of both CRAF and ARAF rescues the CRAF-loss phenotype. Mechanistically, CRAF depletion causes sustained ERK activation and induction of cell-cycle arrest, while treatment with low-dose MEK or ERK inhibitor rescues the CRAF-loss phenotype. Our studies highlight the role of CRAF in regulating MAPK signal intensity to promote tumorigenesis downstream of mutant KRAS and suggest that disrupting CRAF dimerization or degrading CRAF may have therapeutic benefit.
Keywords	KRAS ; CRAF ; BRAF ; ARAF ; MAPK ; MEK ; Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2022-02-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: Neutrophils promote VLA-4-dependent B cell antigen presentation and accumulation within the meninges during neuroinflammation.

Parker Harp, Chelsea R / Archambault, Angela S / Cheung, Matthew / Williams, Jesse W / Czepielewski, Rafael S / Duncker, Patrick C / Kilgore, Aaron J / Miller, Aidan T / Segal, Benjamin M / Kim, Alfred H J / Randolph, Gwendalyn J / Wu, Gregory F

Proceedings of the National Academy of Sciences of the United States of America

2019 Volume 116, Issue 48, Page(s) 24221–24230

Abstract: The success of B cell depletion therapies and identification of leptomeningeal ectopic lymphoid tissue (ELT) in patients with multiple sclerosis (MS) has renewed interest in the antibody-independent pathogenic functions of B cells during ... ...

Abstract	The success of B cell depletion therapies and identification of leptomeningeal ectopic lymphoid tissue (ELT) in patients with multiple sclerosis (MS) has renewed interest in the antibody-independent pathogenic functions of B cells during neuroinflammation. The timing and location of B cell antigen presentation during MS and its animal model experimental autoimmune encephalomyelitis (EAE) remain undefined. Using a new EAE system that incorporates temporal regulation of MHCII expression by myelin-specific B cells, we observed the rapid formation of large B cell clusters in the spinal cord subarachnoid space. Neutrophils preceded the accumulation of meningeal B cell clusters, and inhibition of CXCR2-mediated granulocyte trafficking to the central nervous system reduced pathogenic B cell clusters and disease severity. Further, B cell-restricted very late antigen-4 (VLA-4) deficiency abrogated EAE dependent on B cell antigen presentation. Together, our findings demonstrate that neutrophils coordinate VLA-4-dependent B cell accumulation within the meninges during neuroinflammation, a key early step in the formation of ELT observed in MS.
MeSH term(s)	Animals ; Antigen Presentation ; B-Lymphocytes/immunology ; B-Lymphocytes/pathology ; Chemokines/metabolism ; Disease Models, Animal ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Encephalomyelitis, Autoimmune, Experimental/pathology ; Female ; Integrin alpha4beta1/immunology ; Integrin alpha4beta1/metabolism ; Lymphoid Tissue/immunology ; Lymphoid Tissue/pathology ; Male ; Meninges/immunology ; Meninges/pathology ; Meningitis/immunology ; Meningitis/pathology ; Mice, Inbred C57BL ; Multiple Sclerosis/immunology ; Multiple Sclerosis/pathology ; Myeloid Cells/pathology ; Neutrophils/immunology ; Neutrophils/pathology ; Rabbits ; Receptors, Interleukin-8B/metabolism ; Subarachnoid Space/pathology
Chemical Substances	Chemokines ; Cxcr2 protein, mouse ; Integrin alpha4beta1 ; Receptors, Interleukin-8B
Language	English
Publishing date	2019-11-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Video-Audio Media
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1909098116
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Article ; Online: Mature myelin maintenance requires Qki to coactivate PPARβ-RXRα-mediated lipid metabolism.

The Journal of clinical investigation

2020 Volume 130, Issue 5, Page(s) 2220–2236

Abstract: Lipid-rich myelin forms electrically insulating, axon-wrapping multilayers that are essential for neural function, and mature myelin is traditionally considered metabolically inert. Surprisingly, we discovered that mature myelin lipids undergo rapid ... ...

Abstract	Lipid-rich myelin forms electrically insulating, axon-wrapping multilayers that are essential for neural function, and mature myelin is traditionally considered metabolically inert. Surprisingly, we discovered that mature myelin lipids undergo rapid turnover, and quaking (Qki) is a major regulator of myelin lipid homeostasis. Oligodendrocyte-specific Qki depletion, without affecting oligodendrocyte survival, resulted in rapid demyelination, within 1 week, and gradually neurological deficits in adult mice. Myelin lipids, especially the monounsaturated fatty acids and very-long-chain fatty acids, were dramatically reduced by Qki depletion, whereas the major myelin proteins remained intact, and the demyelinating phenotypes of Qki-depleted mice were alleviated by a high-fat diet. Mechanistically, Qki serves as a coactivator of the PPARβ-RXRα complex, which controls the transcription of lipid-metabolism genes, particularly those involved in fatty acid desaturation and elongation. Treatment of Qki-depleted mice with PPARβ/RXR agonists significantly alleviated neurological disability and extended survival durations. Furthermore, a subset of lesions from patients with primary progressive multiple sclerosis were characterized by preferential reductions in myelin lipid contents, activities of various lipid metabolism pathways, and expression level of QKI-5 in human oligodendrocytes. Together, our results demonstrate that continuous lipid synthesis is indispensable for mature myelin maintenance and highlight an underappreciated role of lipid metabolism in demyelinating diseases.
MeSH term(s)	Animals ; DNA-Binding Proteins/antagonists & inhibitors ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Demyelinating Diseases/genetics ; Demyelinating Diseases/metabolism ; Demyelinating Diseases/pathology ; Fatty Acids/genetics ; Fatty Acids/metabolism ; Humans ; Lipid Metabolism ; Mice ; Mice, Knockout ; Myelin Sheath/genetics ; Myelin Sheath/metabolism ; Myelin Sheath/pathology ; Oligodendroglia/metabolism ; Oligodendroglia/pathology ; PPAR-beta/antagonists & inhibitors ; PPAR-beta/genetics ; PPAR-beta/metabolism ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism
Chemical Substances	DNA-Binding Proteins ; Fatty Acids ; PPAR-beta ; Qk protein, mouse ; RNA-Binding Proteins ; Rxrb protein, mouse
Language	English
Publishing date	2020-03-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI131800
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Article ; Online: Effect of Template Reporting of Brain MRIs for Multiple Sclerosis on Report Thoroughness and Neurologist-Rated Quality: Results of a Prospective Quality Improvement Project.

Dickerson, Elliot / Davenport, Matthew S / Syed, Faiz / Stuve, Olaf / Cohen, Jeffrey A / Rinker, John R / Goldman, Myla D / Segal, Benjamin M / Foerster, Bradley R

Journal of the American College of Radiology : JACR

2017 Volume 14, Issue 3, Page(s) 371–379.e1

Abstract: Purpose: To assess the impact of structured reporting templates on the objective and subjective quality of radiology reports for brain MRIs in patients with multiple sclerosis (MS).: Methods: A HIPAA-compliant prospective quality improvement ... ...

Abstract	Purpose: To assess the impact of structured reporting templates on the objective and subjective quality of radiology reports for brain MRIs in patients with multiple sclerosis (MS). Methods: A HIPAA-compliant prospective quality improvement initiative was undertaken to develop and implement a 12-item structured reporting template for brain MRI examinations in patients with known or suspected MS based on published guidelines. Reports created 1 year before implementing the template served as the baseline. A random sample of 10 template and 10 non-template reports was sent to five neurologists outside the study institution with MS expertise, who reviewed the reports for comprehensiveness and quality. The number of MS-relevant elements in template and non-template reports were compared with unpaired t tests. Proportions were compared with χ Results: There were 63 reports in the pre-template period and 93 reports in the post-template period. Use of the template increased over time in the post-template period (P = .04). All 12 MS-relevant findings were addressed more often and with less variability in template reports: (11.1 ± 0.7 findings versus 5.8 ± 2.2 findings in non-template reports, P < .001). Neurologists were more likely to give the template reports the highest positive rating (56% [107/190] versus 28% [56/199], P < .001) and less likely to give the template reports a lower rating (7% [13/190] versus 15% [29/199], P = .01) compared with the non-template reports. Conclusion: Template reporting of brain MRI examinations increases the rate at which MS-relevant findings are included in the report. Standardized reports are preferred by neurologists with MS expertise.
MeSH term(s)	Adult ; Aged ; Documentation/standards ; Female ; Humans ; Magnetic Resonance Imaging/standards ; Male ; Middle Aged ; Multiple Sclerosis/diagnostic imaging ; Neuroimaging/standards ; Neurologists ; Prospective Studies ; Quality Improvement ; United States
Language	English
Publishing date	2017-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2274861-1
ISSN	1558-349X ; 1546-1440
ISSN (online)	1558-349X
ISSN	1546-1440
DOI	10.1016/j.jacr.2016.09.037
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Article: Microbial signatures in the lower airways of mechanically ventilated COVID19 patients associated with poor clinical outcome.

Sulaiman, Imran / Chung, Matthew / Angel, Luis / Koralov, Sergei / Wu, Benjamin / Yeung, Stephen / Krolikowski, Kelsey / Li, Yonghua / Duerr, Ralf / Schluger, Rosemary / Thannickal, Sara / Koide, Akiko / Rafeq, Samaan / Barnett, Clea / Postelnicu, Radu / Wang, Chang / Banakis, Stephanie / Perez-Perez, Lizzette / Jour, George /

Shen, Guomiao / Meyn, Peter / Carpenito, Joseph / Liu, Xiuxiu / Ji, Kun / Collazo, Destiny / Labarbiera, Anthony / Amoroso, Nancy / Brosnahan, Shari / Mukherjee, Vikramjit / Kaufman, David / Bakker, Jan / Lubinsky, Anthony / Pradhan, Deepak / Sterman, Daniel / Heguy, Adriana / Uyeki, Timothy / Clemente, Jose / de Wit, Emmie / Schmidt, Ann Marie / Shopsin, Bo / Desvignes, Ludovic / Wang, Chan / Li, Huilin / Zhang, Bin / Forst, Christian / Koide, Shohei / Stapleford, Kenneth / Khanna, Kamal / Ghedin, Elodie / Weiden, Michael / Segal, Leopoldo

Research square

2021

Abstract: Mortality among patients with COVID-19 and respiratory failure is high and there are no known lower airway biomarkers that predict clinical outcome. We investigated whether bacterial respiratory infections and viral load were associated with poor ... ...

Abstract	Mortality among patients with COVID-19 and respiratory failure is high and there are no known lower airway biomarkers that predict clinical outcome. We investigated whether bacterial respiratory infections and viral load were associated with poor clinical outcome and host immune tone. We obtained bacterial and fungal culture data from 589 critically ill subjects with COVID-19 requiring mechanical ventilation. On a subset of the subjects that underwent bronchoscopy, we also quantified SARS-CoV-2 viral load, analyzed the microbiome of the lower airways by metagenome and metatranscriptome analyses and profiled the host immune response. We found that isolation of a hospital-acquired respiratory pathogen was not associated with fatal outcome. However, poor clinical outcome was associated with enrichment of the lower airway microbiota with an oral commensal (
Language	English
Publishing date	2021-03-29
Publishing country	United States
Document type	Preprint
DOI	10.21203/rs.3.rs-266050/v1
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