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8 results on '"NHLBI LungMap Consortium"'

1. Guided construction of single cell reference for human and mouse lung

Author

Minzhe Guo, Michael P. Morley, Cheng Jiang, Yixin Wu, Guangyuan Li, Yina Du, Shuyang Zhao, Andrew Wagner, Adnan Cihan Cakar, Michal Kouril, Kang Jin, Nathan Gaddis, Joseph A. Kitzmiller, Kathleen Stewart, Maria C. Basil, Susan M. Lin, Yun Ying, Apoorva Babu, Kathryn A. Wikenheiser-Brokamp, Kyu Shik Mun, Anjaparavanda P. Naren, Geremy Clair, Joshua N. Adkins, Gloria S. Pryhuber, Ravi S. Misra, Bruce J. Aronow, Timothy L. Tickle, Nathan Salomonis, Xin Sun, Edward E. Morrisey, Jeffrey A. Whitsett, NHLBI LungMAP Consortium, and Yan Xu

Subjects
Science
Abstract

Abstract Accurate cell type identification is a key and rate-limiting step in single-cell data analysis. Single-cell references with comprehensive cell types, reproducible and functionally validated cell identities, and common nomenclatures are much needed by the research community for automated cell type annotation, data integration, and data sharing. Here, we develop a computational pipeline utilizing the LungMAP CellCards as a dictionary to consolidate single-cell transcriptomic datasets of 104 human lungs and 17 mouse lung samples to construct LungMAP single-cell reference (CellRef) for both normal human and mouse lungs. CellRefs define 48 human and 40 mouse lung cell types catalogued from diverse anatomic locations and developmental time points. We demonstrate the accuracy and stability of LungMAP CellRefs and their utility for automated cell type annotation of both normal and diseased lungs using multiple independent methods and testing data. We develop user-friendly web interfaces for easy access and maximal utilization of the LungMAP CellRefs.

Published
2023
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2. Single-cell multiomic profiling of human lungs reveals cell-type-specific and age-dynamic control of SARS-CoV2 host genes

Author

Allen Wang, Joshua Chiou, Olivier B Poirion, Justin Buchanan, Michael J Valdez, Jamie M Verheyden, Xiaomeng Hou, Parul Kudtarkar, Sharvari Narendra, Jacklyn M Newsome, Minzhe Guo, Dina A Faddah, Kai Zhang, Randee E Young, Justinn Barr, Eniko Sajti, Ravi Misra, Heidie Huyck, Lisa Rogers, Cory Poole, Jeffery A Whitsett, Gloria Pryhuber, Yan Xu, Kyle J Gaulton, Sebastian Preissl, Xin Sun, and NHLBI LungMap Consortium

Subjects
lung, gene regulation, single cell RNA/ATAC-seq, cis-regulatory elements, human sequence variants, COVID-19, Medicine, Science, Biology (General), QH301-705.5
Abstract

Respiratory failure associated with COVID-19 has placed focus on the lungs. Here, we present single-nucleus accessible chromatin profiles of 90,980 nuclei and matched single-nucleus transcriptomes of 46,500 nuclei in non-diseased lungs from donors of ~30 weeks gestation,~3 years and ~30 years. We mapped candidate cis-regulatory elements (cCREs) and linked them to putative target genes. We identified distal cCREs with age-increased activity linked to SARS-CoV-2 host entry gene TMPRSS2 in alveolar type 2 cells, which had immune regulatory signatures and harbored variants associated with respiratory traits. At the 3p21.31 COVID-19 risk locus, a candidate variant overlapped a distal cCRE linked to SLC6A20, a gene expressed in alveolar cells and with known functional association with the SARS-CoV-2 receptor ACE2. Our findings provide insight into regulatory logic underlying genes implicated in COVID-19 in individual lung cell types across age. More broadly, these datasets will facilitate interpretation of risk loci for lung diseases.

Published
2020
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3. Single-cell multiomic profiling of human lungs reveals cell-type-specific and age-dynamic control of SARS-CoV2 host genes.

Author

Wang, Allen, Chiou, Joshua, Poirion, Olivier B, Buchanan, Justin, Valdez, Michael J, Verheyden, Jamie M, Hou, Xiaomeng, Kudtarkar, Parul, Narendra, Sharvari, Newsome, Jacklyn M, Guo, Minzhe, Faddah, Dina A, Zhang, Kai, Young, Randee E, Barr, Justinn, Sajti, Eniko, Misra, Ravi, Huyck, Heidie, Rogers, Lisa, Poole, Cory, Whitsett, Jeffery A, Pryhuber, Gloria, Xu, Yan, Gaulton, Kyle J, Preissl, Sebastian, Sun, Xin, and NHLBI LungMap Consortium

Subjects
NHLBI LungMap Consortium, Lung, Humans, Membrane Transport Proteins, Receptors, Virus, Chromosome Mapping, Gene Expression Profiling, Age Factors, Adult, Child, Preschool, Infant, Newborn, Virus Internalization, Genetic Variation, Pandemics, Single-Cell Analysis, Alveolar Epithelial Cells, Host Microbial Interactions, COVID-19, Angiotensin-Converting Enzyme 2, SARS-CoV-2, cis-regulatory elements, developmental biology, gene regulation, genetics, genomics, human, human sequence variants, lung, single cell RNA/ATAC-seq, Receptors, Virus, Child, Preschool, Infant, Newborn, Biochemistry and Cell Biology
Abstract

Respiratory failure associated with COVID-19 has placed focus on the lungs. Here, we present single-nucleus accessible chromatin profiles of 90,980 nuclei and matched single-nucleus transcriptomes of 46,500 nuclei in non-diseased lungs from donors of ~30 weeks gestation,~3 years and ~30 years. We mapped candidate cis-regulatory elements (cCREs) and linked them to putative target genes. We identified distal cCREs with age-increased activity linked to SARS-CoV-2 host entry gene TMPRSS2 in alveolar type 2 cells, which had immune regulatory signatures and harbored variants associated with respiratory traits. At the 3p21.31 COVID-19 risk locus, a candidate variant overlapped a distal cCRE linked to SLC6A20, a gene expressed in alveolar cells and with known functional association with the SARS-CoV-2 receptor ACE2. Our findings provide insight into regulatory logic underlying genes implicated in COVID-19 in individual lung cell types across age. More broadly, these datasets will facilitate interpretation of risk loci for lung diseases.

Published
2020

5. Single-cell meta-analysis of SARS-CoV-2 entry genes across tissues and demographics.

Author

Muus, C, Luecken, MD, Eraslan, G, Sikkema, L, Waghray, A, Heimberg, G, Kobayashi, Y, Vaishnav, ED, Subramanian, A, Smillie, C, Jagadeesh, KA, Duong, ET, Fiskin, E, Triglia, ET, Ansari, M, Cai, P, Lin, B, Buchanan, J, Chen, S, Shu, J, Haber, AL, Chung, H, Montoro, DT, Adams, T, Aliee, H, Allon, SJ, Andrusivova, Z, Angelidis, I, Ashenberg, O, Bassler, K, Bécavin, C, Benhar, I, Bergenstråhle, J, Bergenstråhle, L, Bolt, L, Braun, E, Bui, LT, Callori, S, Chaffin, M, Chichelnitskiy, E, Chiou, J, Conlon, TM, Cuoco, MS, Cuomo, ASE, Deprez, M, Duclos, G, Fine, D, Fischer, DS, Ghazanfar, S, Gillich, A, Giotti, B, Gould, J, Guo, M, Gutierrez, AJ, Habermann, AC, Harvey, T, He, P, Hou, X, Hu, L, Hu, Y, Jaiswal, A, Ji, L, Jiang, P, Kapellos, TS, Kuo, CS, Larsson, L, Leney-Greene, MA, Lim, K, Litviňuková, M, Ludwig, LS, Lukassen, S, Luo, W, Maatz, H, Madissoon, E, Mamanova, L, Manakongtreecheep, K, Leroy, S, Mayr, CH, Mbano, IM, McAdams, AM, Nabhan, AN, Nyquist, SK, Penland, L, Poirion, OB, Poli, S, Qi, C, Queen, R, Reichart, D, Rosas, I, Schupp, JC, Shea, CV, Shi, X, Sinha, R, Sit, RV, Slowikowski, K, Slyper, M, Smith, NP, Sountoulidis, A, Strunz, M, Sullivan, TB, Sun, D, Talavera-López, C, Tan, P, Tantivit, J, Travaglini, KJ, Tucker, NR, Vernon, KA, Wadsworth, MH, Waldman, J, Wang, X, Xu, K, Yan, W, Zhao, W, Ziegler, CGK, NHLBI LungMap Consortium, Human Cell Atlas Lung Biological Network, Muus, C, Luecken, MD, Eraslan, G, Sikkema, L, Waghray, A, Heimberg, G, Kobayashi, Y, Vaishnav, ED, Subramanian, A, Smillie, C, Jagadeesh, KA, Duong, ET, Fiskin, E, Triglia, ET, Ansari, M, Cai, P, Lin, B, Buchanan, J, Chen, S, Shu, J, Haber, AL, Chung, H, Montoro, DT, Adams, T, Aliee, H, Allon, SJ, Andrusivova, Z, Angelidis, I, Ashenberg, O, Bassler, K, Bécavin, C, Benhar, I, Bergenstråhle, J, Bergenstråhle, L, Bolt, L, Braun, E, Bui, LT, Callori, S, Chaffin, M, Chichelnitskiy, E, Chiou, J, Conlon, TM, Cuoco, MS, Cuomo, ASE, Deprez, M, Duclos, G, Fine, D, Fischer, DS, Ghazanfar, S, Gillich, A, Giotti, B, Gould, J, Guo, M, Gutierrez, AJ, Habermann, AC, Harvey, T, He, P, Hou, X, Hu, L, Hu, Y, Jaiswal, A, Ji, L, Jiang, P, Kapellos, TS, Kuo, CS, Larsson, L, Leney-Greene, MA, Lim, K, Litviňuková, M, Ludwig, LS, Lukassen, S, Luo, W, Maatz, H, Madissoon, E, Mamanova, L, Manakongtreecheep, K, Leroy, S, Mayr, CH, Mbano, IM, McAdams, AM, Nabhan, AN, Nyquist, SK, Penland, L, Poirion, OB, Poli, S, Qi, C, Queen, R, Reichart, D, Rosas, I, Schupp, JC, Shea, CV, Shi, X, Sinha, R, Sit, RV, Slowikowski, K, Slyper, M, Smith, NP, Sountoulidis, A, Strunz, M, Sullivan, TB, Sun, D, Talavera-López, C, Tan, P, Tantivit, J, Travaglini, KJ, Tucker, NR, Vernon, KA, Wadsworth, MH, Waldman, J, Wang, X, Xu, K, Yan, W, Zhao, W, Ziegler, CGK, NHLBI LungMap Consortium, and Human Cell Atlas Lung Biological Network

Abstract

Angiotensin-converting enzyme 2 (ACE2) and accessory proteases (TMPRSS2 and CTSL) are needed for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) cellular entry, and their expression may shed light on viral tropism and impact across the body. We assessed the cell-type-specific expression of ACE2, TMPRSS2 and CTSL across 107 single-cell RNA-sequencing studies from different tissues. ACE2, TMPRSS2 and CTSL are coexpressed in specific subsets of respiratory epithelial cells in the nasal passages, airways and alveoli, and in cells from other organs associated with coronavirus disease 2019 (COVID-19) transmission or pathology. We performed a meta-analysis of 31 lung single-cell RNA-sequencing studies with 1,320,896 cells from 377 nasal, airway and lung parenchyma samples from 228 individuals. This revealed cell-type-specific associations of age, sex and smoking with expression levels of ACE2, TMPRSS2 and CTSL. Expression of entry factors increased with age and in males, including in airway secretory cells and alveolar type 2 cells. Expression programs shared by ACE2+TMPRSS2+ cells in nasal, lung and gut tissues included genes that may mediate viral entry, key immune functions and epithelial-macrophage cross-talk, such as genes involved in the interleukin-6, interleukin-1, tumor necrosis factor and complement pathways. Cell-type-specific expression patterns may contribute to the pathogenesis of COVID-19, and our work highlights putative molecular pathways for therapeutic intervention.

Published
2021

6. Single-cell meta-analysis of SARS-CoV-2 entry genes across tissues and demographics

Author

Muus, C, Luecken, MD, Eraslan, G, Sikkema, L, Waghray, A, Heimberg, G, Kobayashi, Y, Vaishnav, ED, Subramanian, A, Smillie, C, Jagadeesh, KA, Duong, ET, Fiskin, E, Triglia, ET, Ansari, M, Cai, P, Lin, B, Buchanan, J, Chen, S, Shu, J, Haber, AL, Chung, H, Montoro, DT, Adams, T, Aliee, H, Allon, SJ, Andrusivova, Z, Angelidis, I, Ashenberg, O, Bassler, K, Bécavin, C, Benhar, I, Bergenstråhle, J, Bergenstråhle, L, Bolt, L, Braun, E, Bui, LT, Callori, S, Chaffin, M, Chichelnitskiy, E, Chiou, J, Conlon, TM, Cuoco, MS, Cuomo, ASE, Deprez, M, Duclos, G, Fine, D, Fischer, DS, Ghazanfar, S, Gillich, A, Giotti, B, Gould, J, Guo, M, Gutierrez, AJ, Habermann, AC, Harvey, T, He, P, Hou, X, Hu, L, Hu, Y, Jaiswal, A, Ji, L, Jiang, P, Kapellos, TS, Kuo, CS, Larsson, L, Leney-Greene, MA, Lim, K, Litviňuková, M, Ludwig, LS, Lukassen, S, Luo, W, Maatz, H, Madissoon, E, Mamanova, L, Manakongtreecheep, K, Leroy, S, Mayr, CH, Mbano, IM, McAdams, AM, Nabhan, AN, Nyquist, SK, Penland, L, Poirion, OB, Poli, S, Qi, C, Queen, R, Reichart, D, Rosas, I, Schupp, JC, Shea, CV, Shi, X, Sinha, R, Sit, RV, Slowikowski, K, Slyper, M, Smith, NP, Sountoulidis, A, Strunz, M, Sullivan, TB, Sun, D, Talavera-López, C, Tan, P, Tantivit, J, Travaglini, KJ, Tucker, NR, Vernon, KA, Wadsworth, MH, Waldman, J, Wang, X, Xu, K, Yan, W, Zhao, W, Ziegler, CGK, NHLBI LungMap Consortium, and Human Cell Atlas Lung Biological Network

Subjects
Adult, Male, Cathepsin L, Immunology, Respiratory System, Datasets as Topic, Humans, Lung, 11 Medical and Health Sciences, Aged, Demography, Aged, 80 and over, SARS-CoV-2, Sequence Analysis, RNA, Gene Expression Profiling, Serine Endopeptidases, COVID-19, respiratory system, Middle Aged, Virus Internalization, Organ Specificity, Alveolar Epithelial Cells, Host-Pathogen Interactions, Female, Angiotensin-Converting Enzyme 2, Single-Cell Analysis
Abstract

Angiotensin-converting enzyme 2 (ACE2) and accessory proteases (TMPRSS2 and CTSL) are needed for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) cellular entry, and their expression may shed light on viral tropism and impact across the body. We assessed the cell-type-specific expression of ACE2, TMPRSS2 and CTSL across 107 single-cell RNA-sequencing studies from different tissues. ACE2, TMPRSS2 and CTSL are coexpressed in specific subsets of respiratory epithelial cells in the nasal passages, airways and alveoli, and in cells from other organs associated with coronavirus disease 2019 (COVID-19) transmission or pathology. We performed a meta-analysis of 31 lung single-cell RNA-sequencing studies with 1,320,896 cells from 377 nasal, airway and lung parenchyma samples from 228 individuals. This revealed cell-type-specific associations of age, sex and smoking with expression levels of ACE2, TMPRSS2 and CTSL. Expression of entry factors increased with age and in males, including in airway secretory cells and alveolar type 2 cells. Expression programs shared by ACE2+TMPRSS2+ cells in nasal, lung and gut tissues included genes that may mediate viral entry, key immune functions and epithelial-macrophage cross-talk, such as genes involved in the interleukin-6, interleukin-1, tumor necrosis factor and complement pathways. Cell-type-specific expression patterns may contribute to the pathogenesis of COVID-19, and our work highlights putative molecular pathways for therapeutic intervention.

Published
2020

7. Determinants of SARS-CoV-2 receptor gene expression in upper and lower airways

Author

Aliee, H, Massip, F, Qi, C, De Biase, MS, Van Nijnatten, J, Kersten, ETG, Kermani, NZ, Khuder, B, Vonk, JM, Vermeulen, RCH, U-BIOPRED study group, Cambridge Lung Cancer Early Detection Programme, INER-Ciencias Mexican Lung Program, NHLBI LungMAP Consortium, Neighbors, M, Tew, GW, Grimbaldeston, M, Ten Hacken, NHT, Hu, S, Guo, Y, Zhang, X, Sun, K, Hiemstra, PS, Ponder, BA, Mäkelä, MJ, Malmström, K, Rintoul, RC, Reyfman, PA, Theis, FJ, Brandsma, CA, Adcock, IM, Timens, W, Xu, CJ, Van den Berge, M, Schwarz, RF, Koppelman, GH, Nawijn, MC, Faiz, A, and Commission of the European Communities

Abstract

The recent outbreak of the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19), has led to a worldwide pandemic. One week after initial symptoms develop, a subset of patients progresses to severe disease, with high mortality and limited treatment options. To design novel interventions aimed at preventing spread of the virus and reducing progression to severe disease, detailed knowledge of the cell types and regulating factors driving cellular entry is urgently needed. Here we assess the expression patterns in genes required for COVID-19 entry into cells and replication, and their regulation by genetic, epigenetic and environmental factors, throughout the respiratory tract using samples collected from the upper (nasal) and lower airways (bronchi). Matched samples from the upper and lower airways show a clear increased expression of these genes in the nose compared to the bronchi and parenchyma. Cellular deconvolution indicates a clear association of these genes with the proportion of secretory epithelial cells. Smoking status was found to increase the majority of COVID-19 related genes including ACE2 and TMPRSS2 but only in the lower airways, which was associated with a significant increase in the predicted proportion of goblet cells in bronchial samples of current smokers. Both acute and second hand smoke were found to increase ACE2 expression in the bronchus. Inhaled corticosteroids decrease ACE2 expression in the lower airways. No significant effect of genetics on ACE2 expression was observed, but a strong association of DNA- methylation with ACE2 and TMPRSS2- mRNA expression was identified in the bronchus.

Published
2020

8. Single-cell meta-analysis of SARS-CoV-2 entry genes across tissues and demographics

Author

Christoph, Muus, Luecken , Malte D., Gökcen, Eraslan, Lisa, Sikkema, Avinash, Waghray, Graham, Heimberg, Yoshihiko, Kobayashi, Eeshit Dhaval Vaishnav, Ayshwarya, Subramanian, Christopher, Smillie, Jagadeesh, Karthik A., Elizabeth Thu Duong, Evgenij, Fiskin, Elena Torlai Triglia, Meshal, Ansari, Peiwen, Cai, Brian, Lin, Justin, Buchanan, Sijia, Chen, Jian, Shu, Haber, Adam L., Hattie, Chung, Montoro, Daniel T., Taylor, Adams, Hananeh, Aliee, Allon, Samuel J., Zaneta, Andrusivova, Ilias, Angelidis, Orr, Ashenberg, Kevin, Bassler, Christophe, Bécavin, Inbal, Benhar, Joseph, Bergenstråhle, Ludvig, Bergenstråhle, Liam, Bolt, Emelie, Braun, Bui, Linh T., Steven, Callori, Mark, Chaffin, Evgeny, Chichelnitskiy, Joshua, Chiou, Conlon, Thomas M., Cuoco, Michael S., Cuomo, Anna S. E., Marie, Deprez, Grant, Duclos, Denise, Fine, Fischer, David S., Shila, Ghazanfar, Astrid, Gillich, Bruno, Giotti, Joshua, Gould, Minzhe, Guo, Gutierrez, Austin J., Habermann, Arun C., Tyler, Harvey, Peng, He, Xiaomeng, Hou, Lijuan, Hu, Yan, Hu, Alok, Jaiswal, Lu, Ji, Peiyong, Jiang, Kapellos, Theodoros S., Kuo, Christin S., Ludvig, Larsson, Leney-Greene, Michael A., Kyungtae, Lim, Monika, Litviňuková, Ludwig, Leif S., Soeren, Lukassen, Wendy, Luo, Henrike, Maatz, Elo, Madissoon, Lira, Mamanova, Kasidet, Manakongtreecheep, Sylvie, Leroy, Mayr, Christoph H., Mbano, Ian M., Mcadams, Alexi M., Nabhan, Ahmad N., Nyquist, Sarah K., Lolita, Penland, Poirion, Olivier B., Sergio, Poli, Cancan, Qi, Rachel, Queen, Daniel, Reichart, Ivan, Rosas, Schupp, Jonas C., Shea, Conor V., Xingyi, Shi, Rahul, Sinha, Sit, Rene V., Kamil, Slowikowski, Michal, Slyper, Smith, Neal P., Alex, Sountoulidis, Maximilian, Strunz, Sullivan, Travis B., Dawei, Sun, Carlos, Talavera-López, Peng, Tan, Jessica, Tantivit, Travaglini, Kyle J., Tucker, Nathan R., Vernon, Katherine A., Wadsworth, Marc H., Julia, Waldman, Xiuting, Wang, Ke, Xu, Wenjun, Yan, William, Zhao, Ziegler, Carly G. K., The NHLBI LungMap Consortium, Zerti, Darin, The Human Cell Atlas Lung Biological Network, and Groningen Research Institute for Asthma and COPD (GRIAC)

Subjects
0301 basic medicine, Male, Cathepsin L, Respiratory System, Datasets as Topic, Lung/metabolism, Sequence Analysis, RNA/methods, Organ Specificity/genetics, 0302 clinical medicine, 80 and over, Respiratory system, Lung, COVID-19/epidemiology, Aged, 80 and over, Serine Endopeptidases, General Medicine, respiratory system, Middle Aged, Host-Pathogen Interactions/genetics, 3. Good health, Angiotensin-Converting Enzyme 2/genetics, medicine.anatomical_structure, Datasets as Topic/statistics & numerical data, Respiratory System/metabolism, Organ Specificity, Cathepsin L/genetics, 030220 oncology & carcinogenesis, Host-Pathogen Interactions, Tumor necrosis factor alpha, Female, Angiotensin-Converting Enzyme 2, Single-Cell Analysis, RNA/methods, Sequence Analysis, Adult, Alveolar Epithelial Cells/metabolism, Serine Endopeptidases/genetics, Biology, General Biochemistry, Genetics and Molecular Biology, Article, 03 medical and health sciences, Immune system, Viral entry, Parenchyma, medicine, Humans, Gene Expression Profiling/statistics & numerical data, Aged, Demography, SARS-CoV-2, Sequence Analysis, RNA, Gene Expression Profiling, Single-Cell Analysis/methods, COVID-19, Virus Internalization, Gene expression profiling, 030104 developmental biology, Alveolar Epithelial Cells, Immunology, Tissue tropism, SARS-CoV-2/physiology
Abstract

Angiotensin-converting enzyme 2 (ACE2) and accessory proteases (TMPRSS2 and CTSL) are needed for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) cellular entry, and their expression may shed light on viral tropism and impact across the body. We assessed the cell-type-specific expression of ACE2, TMPRSS2 and CTSL across 107 single-cell RNA-sequencing studies from different tissues. ACE2, TMPRSS2 and CTSL are coexpressed in specific subsets of respiratory epithelial cells in the nasal passages, airways and alveoli, and in cells from other organs associated with coronavirus disease 2019 (COVID-19) transmission or pathology. We performed a meta-analysis of 31 lung single-cell RNA-sequencing studies with 1,320,896 cells from 377 nasal, airway and lung parenchyma samples from 228 individuals. This revealed cell-type-specific associations of age, sex and smoking with expression levels of ACE2, TMPRSS2 and CTSL. Expression of entry factors increased with age and in males, including in airway secretory cells and alveolar type 2 cells. Expression programs shared by ACE2+TMPRSS2+ cells in nasal, lung and gut tissues included genes that may mediate viral entry, key immune functions and epithelial-macrophage cross-talk, such as genes involved in the interleukin-6, interleukin-1, tumor necrosis factor and complement pathways. Cell-type-specific expression patterns may contribute to the pathogenesis of COVID-19, and our work highlights putative molecular pathways for therapeutic intervention.

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