Multimodal single-cell omics analysis identifies epithelium-immune cell interactions and immune vulnerability associated with sex differences in COVID-19.


Journal

Signal transduction and targeted therapy
ISSN: 2059-3635
Titre abrégé: Signal Transduct Target Ther
Pays: England
ID NLM: 101676423

Informations de publication

Date de publication:
30 07 2021
Historique:
received: 08 12 2020
accepted: 13 07 2021
revised: 25 06 2021
entrez: 31 7 2021
pubmed: 1 8 2021
medline: 10 8 2021
Statut: epublish

Résumé

Sex differences in the susceptibility of SARS-CoV-2 infection and severity have been controversial, and the underlying mechanisms of COVID-19 in a sex-specific manner remain understudied. Here we inspected sex differences in SARS-CoV-2 infection, hospitalization, admission to the intensive care unit (ICU), sera inflammatory biomarker profiling, and single-cell RNA-sequencing (scRNA-seq) profiles across nasal, bronchoalveolar lavage fluid (BALF), and peripheral blood mononuclear cells (PBMCs) from COVID-19 patients with varying degrees of disease severities. Our propensity score-matching observations revealed that male individuals have a 29% elevated likelihood of SARS-CoV-2 positivity, with a hazard ratio (HR) 1.32 (95% confidence interval [CI] 1.18-1.48) for hospitalization and HR 1.51 (95% CI 1.24-1.84) for admission to ICU. Sera from male patients at hospital admission had elevated neutrophil-lymphocyte ratio and elevated expression of inflammatory markers (C-reactive protein and procalcitonin). We found that SARS-CoV-2 entry factors, including ACE2, TMPRSS2, FURIN, and NRP1, have elevated expression in nasal squamous cells from male individuals with moderate and severe COVID-19. We observed male-biased transcriptional activation in SARS-CoV-2-infected macrophages from BALF and sputum samples, which offers potential molecular mechanism for sex-biased susceptibility to viral infection. Cell-cell interaction network analysis reveals potential epithelium-immune cell interactions and immune vulnerability underlying male-elevated disease severity and mortality in COVID-19. Mechanistically, monocyte-elevated expression of Toll-like receptor 7 (TLR7) and Bruton tyrosine kinase (BTK) is associated with severe outcomes in males with COVID-19. In summary, these findings provide basis to decipher immune responses underlying sex differences and designing sex-specific targeted interventions and patient care for COVID-19.

Identifiants

pubmed: 34330889
doi: 10.1038/s41392-021-00709-x
pii: 10.1038/s41392-021-00709-x
pmc: PMC8322111
doi:

Types de publication

Clinical Trial Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

292

Subventions

Organisme : Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.)
ID : R01AG066707
Organisme : NHLBI NIH HHS
ID : R00 HL138272
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS109742
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG066707
Pays : United States
Organisme : NCI NIH HHS
ID : P01 CA245705
Pays : United States
Organisme : Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.)
ID : 3R01AG066707-01S1

Informations de copyright

© 2021. The Author(s).

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Auteurs

Yuan Hou (Y)

Genomic Medicine Institute, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.

Yadi Zhou (Y)

Genomic Medicine Institute, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.

Michaela U Gack (MU)

Florida Research and Innovation Center, Cleveland Clinic, Port Saint Lucie, FL, USA.

Justin D Lathia (JD)

Department of Cardiovascular and Metabolic Science, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, USA.

Asha Kallianpur (A)

Genomic Medicine Institute, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, USA.
Department of Population and Quantitative Health Sciences, Case Western Reserve University, Cleveland, OH, USA.

Reena Mehra (R)

Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, USA.
Neurological Institute, Cleveland Clinic, Cleveland, OH, USA.

Timothy A Chan (TA)

Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, USA.
Center for Immunotherapy and Precision Immuno-Oncology, Cleveland Clinic, Cleveland, OH, USA.

Jae U Jung (JU)

Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, USA.
Department of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.

Lara Jehi (L)

Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, USA.
Neurological Institute, Cleveland Clinic, Cleveland, OH, USA.

Charis Eng (C)

Genomic Medicine Institute, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, USA.
Department of Genetics and Genome Sciences, Case Western Reserve University School of Medicine, Cleveland, OH, USA.
Case Comprehensive Cancer Center, Case Western Reserve University School of Medicine, Cleveland, OH, USA.

Feixiong Cheng (F)

Genomic Medicine Institute, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA. chengf@ccf.org.
Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, USA. chengf@ccf.org.
Case Comprehensive Cancer Center, Case Western Reserve University School of Medicine, Cleveland, OH, USA. chengf@ccf.org.

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