Δ9-Tetrahydrocannabinol Prevents Mortality from Acute Respiratory Distress Syndrome through the Induction of Apoptosis in Immune Cells, Leading to Cytokine Storm Suppression.
Identifieur interne : 000046 ( Main/Exploration ); précédent : 000045; suivant : 000047Δ9-Tetrahydrocannabinol Prevents Mortality from Acute Respiratory Distress Syndrome through the Induction of Apoptosis in Immune Cells, Leading to Cytokine Storm Suppression.
Auteurs : Amira Mohammed [États-Unis] ; Hasan F K Alghetaa [États-Unis] ; Kathryn Miranda [États-Unis] ; Kiesha Wilson [États-Unis] ; Narendra P Singh [États-Unis] ; Guoshuai Cai [États-Unis] ; Nagireddy Putluri [États-Unis] ; Prakash Nagarkatti [États-Unis] ; Mitzi Nagarkatti [États-Unis]Source :
- International journal of molecular sciences [ 1422-0067 ] ; 2020.
Descripteurs français
- KwdFr :
- Adulte d'âge moyen (MeSH), Agonistes des récepteurs de cannabinoïdes (usage thérapeutique), Animaux (MeSH), Apoptose (effets des médicaments et des substances chimiques), Betacoronavirus (physiologie), Cytokines (immunologie), Dronabinol (usage thérapeutique), Entérotoxines (effets indésirables), Femelle (MeSH), Humains (MeSH), Infections à coronavirus (mortalité), Infections à coronavirus (traitement médicamenteux), Infections à coronavirus (virologie), Liquide de lavage bronchoalvéolaire (immunologie), Mâle (MeSH), Pandémies (MeSH), Pneumopathie infectieuse (traitement médicamenteux), Pneumopathie infectieuse (virologie), Pneumopathie virale (mortalité), Pneumopathie virale (traitement médicamenteux), Pneumopathie virale (virologie), Poumon (immunologie), Poumon (virologie), Souris (MeSH), Souris de lignée C3H (MeSH), Sujet âgé (MeSH), Syndrome de détresse respiratoire de l'adulte (mortalité), Syndrome de détresse respiratoire de l'adulte (traitement médicamenteux), Syndrome de détresse respiratoire de l'adulte (virologie), Transduction du signal (effets des médicaments et des substances chimiques), microARN (génétique).
- MESH :
- effets des médicaments et des substances chimiques : Apoptose, Transduction du signal.
- effets indésirables : Entérotoxines.
- génétique : microARN.
- immunologie : Cytokines, Liquide de lavage bronchoalvéolaire, Poumon.
- mortalité : Infections à coronavirus, Pneumopathie virale, Syndrome de détresse respiratoire de l'adulte.
- physiologie : Betacoronavirus.
- traitement médicamenteux : Infections à coronavirus, Pneumopathie infectieuse, Pneumopathie virale, Syndrome de détresse respiratoire de l'adulte.
- usage thérapeutique : Agonistes des récepteurs de cannabinoïdes, Dronabinol.
- virologie : Infections à coronavirus, Pneumopathie infectieuse, Pneumopathie virale, Poumon, Syndrome de détresse respiratoire de l'adulte.
- Adulte d'âge moyen, Animaux, Femelle, Humains, Mâle, Pandémies, Souris, Souris de lignée C3H, Sujet âgé.
English descriptors
- KwdEn :
- Aged (MeSH), Animals (MeSH), Apoptosis (drug effects), Betacoronavirus (physiology), Bronchoalveolar Lavage Fluid (immunology), Cannabinoid Receptor Agonists (therapeutic use), Coronavirus Infections (drug therapy), Coronavirus Infections (mortality), Coronavirus Infections (virology), Cytokines (immunology), Dronabinol (therapeutic use), Enterotoxins (adverse effects), Female (MeSH), Humans (MeSH), Lung (immunology), Lung (virology), Male (MeSH), Mice (MeSH), Mice, Inbred C3H (MeSH), MicroRNAs (genetics), Middle Aged (MeSH), Pandemics (MeSH), Pneumonia (drug therapy), Pneumonia (virology), Pneumonia, Viral (drug therapy), Pneumonia, Viral (mortality), Pneumonia, Viral (virology), Respiratory Distress Syndrome, Adult (drug therapy), Respiratory Distress Syndrome, Adult (mortality), Respiratory Distress Syndrome, Adult (virology), Signal Transduction (drug effects).
- MESH :
- chemical , adverse effects : Enterotoxins.
- chemical , genetics : MicroRNAs.
- chemical , immunology : Cytokines.
- chemical , therapeutic use : Cannabinoid Receptor Agonists, Dronabinol.
- drug effects : Apoptosis, Signal Transduction.
- drug therapy : Coronavirus Infections, Pneumonia, Pneumonia, Viral, Respiratory Distress Syndrome, Adult.
- immunology : Bronchoalveolar Lavage Fluid, Lung.
- mortality : Coronavirus Infections, Pneumonia, Viral, Respiratory Distress Syndrome, Adult.
- physiology : Betacoronavirus.
- virology : Coronavirus Infections, Lung, Pneumonia, Pneumonia, Viral, Respiratory Distress Syndrome, Adult.
- Aged, Animals, Female, Humans, Male, Mice, Mice, Inbred C3H, Middle Aged, Pandemics.
Abstract
Acute Respiratory Distress Syndrome (ARDS) causes up to 40% mortality in humans and is difficult to treat. ARDS is also one of the major triggers of mortality associated with coronavirus-induced disease (COVID-19). We used a mouse model of ARDS induced by Staphylococcal enterotoxin B (SEB), which triggers 100% mortality, to investigate the mechanisms through which Δ9-tetrahydrocannabinol (THC) attenuates ARDS. SEB was used to trigger ARDS in C3H mice. These mice were treated with THC and analyzed for survival, ARDS, cytokine storm, and metabolome. Additionally, cells isolated from the lungs were used to perform single-cell RNA sequencing and transcriptome analysis. A database analysis of human COVID-19 patients was also performed to compare the signaling pathways with SEB-mediated ARDS. The treatment of SEB-mediated ARDS mice with THC led to a 100% survival, decreased lung inflammation, and the suppression of cytokine storm. This was associated with immune cell apoptosis involving the mitochondrial pathway, as suggested by single-cell RNA sequencing. A transcriptomic analysis of immune cells from the lungs revealed an increase in mitochondrial respiratory chain enzymes following THC treatment. In addition, metabolomic analysis revealed elevated serum concentrations of amino acids, lysine, n-acetyl methionine, carnitine, and propionyl L-carnitine in THC-treated mice. THC caused the downregulation of miR-185, which correlated with an increase in the pro-apoptotic gene targets. Interestingly, the gene expression datasets from the bronchoalveolar lavage fluid (BALF) of human COVID-19 patients showed some similarities between cytokine and apoptotic genes with SEB-induced ARDS. Collectively, this study suggests that the activation of cannabinoid receptors may serve as a therapeutic modality to treat ARDS associated with COVID-19.
DOI: 10.3390/ijms21176244
PubMed: 32872332
PubMed Central: PMC7503745
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged (MeSH)</term>
<term>Animals (MeSH)</term>
<term>Apoptosis (drug effects)</term>
<term>Betacoronavirus (physiology)</term>
<term>Bronchoalveolar Lavage Fluid (immunology)</term>
<term>Cannabinoid Receptor Agonists (therapeutic use)</term>
<term>Coronavirus Infections (drug therapy)</term>
<term>Coronavirus Infections (mortality)</term>
<term>Coronavirus Infections (virology)</term>
<term>Cytokines (immunology)</term>
<term>Dronabinol (therapeutic use)</term>
<term>Enterotoxins (adverse effects)</term>
<term>Female (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Lung (immunology)</term>
<term>Lung (virology)</term>
<term>Male (MeSH)</term>
<term>Mice (MeSH)</term>
<term>Mice, Inbred C3H (MeSH)</term>
<term>MicroRNAs (genetics)</term>
<term>Middle Aged (MeSH)</term>
<term>Pandemics (MeSH)</term>
<term>Pneumonia (drug therapy)</term>
<term>Pneumonia (virology)</term>
<term>Pneumonia, Viral (drug therapy)</term>
<term>Pneumonia, Viral (mortality)</term>
<term>Pneumonia, Viral (virology)</term>
<term>Respiratory Distress Syndrome, Adult (drug therapy)</term>
<term>Respiratory Distress Syndrome, Adult (mortality)</term>
<term>Respiratory Distress Syndrome, Adult (virology)</term>
<term>Signal Transduction (drug effects)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Adulte d'âge moyen (MeSH)</term>
<term>Agonistes des récepteurs de cannabinoïdes (usage thérapeutique)</term>
<term>Animaux (MeSH)</term>
<term>Apoptose (effets des médicaments et des substances chimiques)</term>
<term>Betacoronavirus (physiologie)</term>
<term>Cytokines (immunologie)</term>
<term>Dronabinol (usage thérapeutique)</term>
<term>Entérotoxines (effets indésirables)</term>
<term>Femelle (MeSH)</term>
<term>Humains (MeSH)</term>
<term>Infections à coronavirus (mortalité)</term>
<term>Infections à coronavirus (traitement médicamenteux)</term>
<term>Infections à coronavirus (virologie)</term>
<term>Liquide de lavage bronchoalvéolaire (immunologie)</term>
<term>Mâle (MeSH)</term>
<term>Pandémies (MeSH)</term>
<term>Pneumopathie infectieuse (traitement médicamenteux)</term>
<term>Pneumopathie infectieuse (virologie)</term>
<term>Pneumopathie virale (mortalité)</term>
<term>Pneumopathie virale (traitement médicamenteux)</term>
<term>Pneumopathie virale (virologie)</term>
<term>Poumon (immunologie)</term>
<term>Poumon (virologie)</term>
<term>Souris (MeSH)</term>
<term>Souris de lignée C3H (MeSH)</term>
<term>Sujet âgé (MeSH)</term>
<term>Syndrome de détresse respiratoire de l'adulte (mortalité)</term>
<term>Syndrome de détresse respiratoire de l'adulte (traitement médicamenteux)</term>
<term>Syndrome de détresse respiratoire de l'adulte (virologie)</term>
<term>Transduction du signal (effets des médicaments et des substances chimiques)</term>
<term>microARN (génétique)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Enterotoxins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>MicroRNAs</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Cytokines</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Cannabinoid Receptor Agonists</term>
<term>Dronabinol</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Coronavirus Infections</term>
<term>Pneumonia</term>
<term>Pneumonia, Viral</term>
<term>Respiratory Distress Syndrome, Adult</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Apoptose</term>
<term>Transduction du signal</term>
</keywords>
<keywords scheme="MESH" qualifier="effets indésirables" xml:lang="fr"><term>Entérotoxines</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>microARN</term>
</keywords>
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<term>Liquide de lavage bronchoalvéolaire</term>
<term>Poumon</term>
</keywords>
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<term>Lung</term>
</keywords>
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<term>Pneumonia, Viral</term>
<term>Respiratory Distress Syndrome, Adult</term>
</keywords>
<keywords scheme="MESH" qualifier="mortalité" xml:lang="fr"><term>Infections à coronavirus</term>
<term>Pneumopathie virale</term>
<term>Syndrome de détresse respiratoire de l'adulte</term>
</keywords>
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<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Betacoronavirus</term>
</keywords>
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<term>Pneumopathie infectieuse</term>
<term>Pneumopathie virale</term>
<term>Syndrome de détresse respiratoire de l'adulte</term>
</keywords>
<keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Agonistes des récepteurs de cannabinoïdes</term>
<term>Dronabinol</term>
</keywords>
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<term>Pneumopathie infectieuse</term>
<term>Pneumopathie virale</term>
<term>Poumon</term>
<term>Syndrome de détresse respiratoire de l'adulte</term>
</keywords>
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<term>Lung</term>
<term>Pneumonia</term>
<term>Pneumonia, Viral</term>
<term>Respiratory Distress Syndrome, Adult</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Aged</term>
<term>Animals</term>
<term>Female</term>
<term>Humans</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred C3H</term>
<term>Middle Aged</term>
<term>Pandemics</term>
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<term>Animaux</term>
<term>Femelle</term>
<term>Humains</term>
<term>Mâle</term>
<term>Pandémies</term>
<term>Souris</term>
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<front><div type="abstract" xml:lang="en">Acute Respiratory Distress Syndrome (ARDS) causes up to 40% mortality in humans and is difficult to treat. ARDS is also one of the major triggers of mortality associated with coronavirus-induced disease (COVID-19). We used a mouse model of ARDS induced by Staphylococcal enterotoxin B (SEB), which triggers 100% mortality, to investigate the mechanisms through which Δ9-tetrahydrocannabinol (THC) attenuates ARDS. SEB was used to trigger ARDS in C3H mice. These mice were treated with THC and analyzed for survival, ARDS, cytokine storm, and metabolome. Additionally, cells isolated from the lungs were used to perform single-cell RNA sequencing and transcriptome analysis. A database analysis of human COVID-19 patients was also performed to compare the signaling pathways with SEB-mediated ARDS. The treatment of SEB-mediated ARDS mice with THC led to a 100% survival, decreased lung inflammation, and the suppression of cytokine storm. This was associated with immune cell apoptosis involving the mitochondrial pathway, as suggested by single-cell RNA sequencing. A transcriptomic analysis of immune cells from the lungs revealed an increase in mitochondrial respiratory chain enzymes following THC treatment. In addition, metabolomic analysis revealed elevated serum concentrations of amino acids, lysine, n-acetyl methionine, carnitine, and propionyl L-carnitine in THC-treated mice. THC caused the downregulation of miR-185, which correlated with an increase in the pro-apoptotic gene targets. Interestingly, the gene expression datasets from the bronchoalveolar lavage fluid (BALF) of human COVID-19 patients showed some similarities between cytokine and apoptotic genes with SEB-induced ARDS. Collectively, this study suggests that the activation of cannabinoid receptors may serve as a therapeutic modality to treat ARDS associated with COVID-19.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">32872332</PMID>
<DateCompleted><Year>2020</Year>
<Month>09</Month>
<Day>11</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>10</Month>
<Day>01</Day>
</DateRevised>
<Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1422-0067</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>21</Volume>
<Issue>17</Issue>
<PubDate><Year>2020</Year>
<Month>Aug</Month>
<Day>28</Day>
</PubDate>
</JournalIssue>
<Title>International journal of molecular sciences</Title>
<ISOAbbreviation>Int J Mol Sci</ISOAbbreviation>
</Journal>
<ArticleTitle>Δ9-Tetrahydrocannabinol Prevents Mortality from Acute Respiratory Distress Syndrome through the Induction of Apoptosis in Immune Cells, Leading to Cytokine Storm Suppression.</ArticleTitle>
<ELocationID EIdType="pii" ValidYN="Y">E6244</ELocationID>
<ELocationID EIdType="doi" ValidYN="Y">10.3390/ijms21176244</ELocationID>
<Abstract><AbstractText>Acute Respiratory Distress Syndrome (ARDS) causes up to 40% mortality in humans and is difficult to treat. ARDS is also one of the major triggers of mortality associated with coronavirus-induced disease (COVID-19). We used a mouse model of ARDS induced by Staphylococcal enterotoxin B (SEB), which triggers 100% mortality, to investigate the mechanisms through which Δ9-tetrahydrocannabinol (THC) attenuates ARDS. SEB was used to trigger ARDS in C3H mice. These mice were treated with THC and analyzed for survival, ARDS, cytokine storm, and metabolome. Additionally, cells isolated from the lungs were used to perform single-cell RNA sequencing and transcriptome analysis. A database analysis of human COVID-19 patients was also performed to compare the signaling pathways with SEB-mediated ARDS. The treatment of SEB-mediated ARDS mice with THC led to a 100% survival, decreased lung inflammation, and the suppression of cytokine storm. This was associated with immune cell apoptosis involving the mitochondrial pathway, as suggested by single-cell RNA sequencing. A transcriptomic analysis of immune cells from the lungs revealed an increase in mitochondrial respiratory chain enzymes following THC treatment. In addition, metabolomic analysis revealed elevated serum concentrations of amino acids, lysine, n-acetyl methionine, carnitine, and propionyl L-carnitine in THC-treated mice. THC caused the downregulation of miR-185, which correlated with an increase in the pro-apoptotic gene targets. Interestingly, the gene expression datasets from the bronchoalveolar lavage fluid (BALF) of human COVID-19 patients showed some similarities between cytokine and apoptotic genes with SEB-induced ARDS. Collectively, this study suggests that the activation of cannabinoid receptors may serve as a therapeutic modality to treat ARDS associated with COVID-19.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mohammed</LastName>
<ForeName>Amira</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Department of Pathology, Microbiology and Immunology, School of Medicine, University of South Carolina, Columbia, SC 29208, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>F K Alghetaa</LastName>
<ForeName>Hasan</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Department of Pathology, Microbiology and Immunology, School of Medicine, University of South Carolina, Columbia, SC 29208, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Miranda</LastName>
<ForeName>Kathryn</ForeName>
<Initials>K</Initials>
<Identifier Source="ORCID">0000-0003-0922-7546</Identifier>
<AffiliationInfo><Affiliation>Department of Pathology, Microbiology and Immunology, School of Medicine, University of South Carolina, Columbia, SC 29208, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wilson</LastName>
<ForeName>Kiesha</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>Department of Pathology, Microbiology and Immunology, School of Medicine, University of South Carolina, Columbia, SC 29208, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>P Singh</LastName>
<ForeName>Narendra</ForeName>
<Initials>N</Initials>
<AffiliationInfo><Affiliation>Department of Pathology, Microbiology and Immunology, School of Medicine, University of South Carolina, Columbia, SC 29208, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Cai</LastName>
<ForeName>Guoshuai</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>Department of Environmental Health Sciences, Arnold School of Public Health, University of South Carolina, Columbia, SC 29208, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Putluri</LastName>
<ForeName>Nagireddy</ForeName>
<Initials>N</Initials>
<AffiliationInfo><Affiliation>Dan L. Duncan Cancer Center, Advanced Technology Core, Alkek Center for Molecular Discovery, Baylor College of Medicine, Houston, TX 77030, USA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Molecular and Cell Biology, Baylor College of Medicine, Houston, TX 77030, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Nagarkatti</LastName>
<ForeName>Prakash</ForeName>
<Initials>P</Initials>
<Identifier Source="ORCID">0000-0003-2663-0759</Identifier>
<AffiliationInfo><Affiliation>Department of Pathology, Microbiology and Immunology, School of Medicine, University of South Carolina, Columbia, SC 29208, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Nagarkatti</LastName>
<ForeName>Mitzi</ForeName>
<Initials>M</Initials>
<Identifier Source="ORCID">0000-0002-5977-5615</Identifier>
<AffiliationInfo><Affiliation>Department of Pathology, Microbiology and Immunology, School of Medicine, University of South Carolina, Columbia, SC 29208, USA.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>P01AT003961</GrantID>
<Acronym>NH</Acronym>
<Agency>NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>P20GM103641</GrantID>
<Acronym>NH</Acronym>
<Agency>NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01AT006888</GrantID>
<Acronym>NH</Acronym>
<Agency>NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01ES030144</GrantID>
<Acronym>NH</Acronym>
<Agency>NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01AI123947</GrantID>
<Acronym>NH</Acronym>
<Agency>NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01AI129788</GrantID>
<Acronym>NH</Acronym>
<Agency>NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01CA220297</GrantID>
<Agency>NIH/NCI</Agency>
<Country></Country>
</Grant>
<Grant><GrantID>R01CA216426</GrantID>
<Agency>NIH/NCI</Agency>
<Country></Country>
</Grant>
<Grant><GrantID>Scholarship to AM</GrantID>
<Agency>MoHESR</Agency>
<Country></Country>
</Grant>
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<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2020</Year>
<Month>08</Month>
<Day>28</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>Switzerland</Country>
<MedlineTA>Int J Mol Sci</MedlineTA>
<NlmUniqueID>101092791</NlmUniqueID>
<ISSNLinking>1422-0067</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D063386">Cannabinoid Receptor Agonists</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D016207">Cytokines</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D004768">Enterotoxins</NameOfSubstance>
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<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C552431">MIRN185 microRNA, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D035683">MicroRNAs</NameOfSubstance>
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<Chemical><RegistryNumber>39424-53-8</RegistryNumber>
<NameOfSubstance UI="C031818">enterotoxin B, staphylococcal</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>7J8897W37S</RegistryNumber>
<NameOfSubstance UI="D013759">Dronabinol</NameOfSubstance>
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<SupplMeshList><SupplMeshName Type="Disease" UI="C000657245">COVID-19</SupplMeshName>
<SupplMeshName Type="Organism" UI="C000656484">severe acute respiratory syndrome coronavirus 2</SupplMeshName>
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<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000073640" MajorTopicYN="N">Betacoronavirus</DescriptorName>
<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001992" MajorTopicYN="N">Bronchoalveolar Lavage Fluid</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D063386" MajorTopicYN="N">Cannabinoid Receptor Agonists</DescriptorName>
<QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018352" MajorTopicYN="N">Coronavirus Infections</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
<QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013759" MajorTopicYN="N">Dronabinol</DescriptorName>
<QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName>
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<MeshHeading><DescriptorName UI="D004768" MajorTopicYN="N">Enterotoxins</DescriptorName>
<QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008168" MajorTopicYN="N">Lung</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008809" MajorTopicYN="N">Mice, Inbred C3H</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D035683" MajorTopicYN="N">MicroRNAs</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D058873" MajorTopicYN="N">Pandemics</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011014" MajorTopicYN="N">Pneumonia</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011024" MajorTopicYN="N">Pneumonia, Viral</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
<QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
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<MeshHeading><DescriptorName UI="D012128" MajorTopicYN="N">Respiratory Distress Syndrome, Adult</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
<QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">acute respiratory distress syndrome</Keyword>
<Keyword MajorTopicYN="N">apoptosis</Keyword>
<Keyword MajorTopicYN="N">cytokine storm</Keyword>
<Keyword MajorTopicYN="N">staphylococcal enterotoxin B</Keyword>
<Keyword MajorTopicYN="N">Δ9-tetrahydrocannabinol</Keyword>
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<Month>08</Month>
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