SARS-CoV2 induced respiratory distress: Can Cannabinoids be added to anti-viral therapies to reduce lung inflammation?
Identifieur interne : 000440 ( Pmc/Corpus ); précédent : 000439; suivant : 000441SARS-CoV2 induced respiratory distress: Can Cannabinoids be added to anti-viral therapies to reduce lung inflammation?
Auteurs : Siddappa N. Byrareddy ; Mahesh MohanSource :
- Brain, Behavior, and Immunity [ 0889-1591 ] ; 2020.
Url:
DOI: 10.1016/j.bbi.2020.04.079
PubMed: NONE
PubMed Central: 7187842
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Byrareddy</name><affiliation><nlm:aff id="af005">Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska 68198, United States</nlm:aff></affiliation></author><author><name sortKey="Mohan, Mahesh" sort="Mohan, Mahesh" uniqKey="Mohan M" first="Mahesh" last="Mohan">Mahesh Mohan</name><affiliation><nlm:aff id="af010">Texas Biomedical Research Institute, Southwest National Primate Research Center, San Antonio, Texas 78227, United States</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmc">7187842</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7187842</idno><idno type="RBID">PMC:7187842</idno><idno type="doi">10.1016/j.bbi.2020.04.079</idno><idno type="pmid">NONE</idno><date when="2020">2020</date><idno type="wicri:Area/Pmc/Corpus">000440</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000440</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">SARS-CoV2 induced respiratory distress: Can Cannabinoids be added to anti-viral therapies to reduce lung inflammation?</title><author><name sortKey="Byrareddy, Siddappa N" sort="Byrareddy, Siddappa N" uniqKey="Byrareddy S" first="Siddappa N." last="Byrareddy">Siddappa N. Byrareddy</name><affiliation><nlm:aff id="af005">Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska 68198, United States</nlm:aff></affiliation></author><author><name sortKey="Mohan, Mahesh" sort="Mohan, Mahesh" uniqKey="Mohan M" first="Mahesh" last="Mohan">Mahesh Mohan</name><affiliation><nlm:aff id="af010">Texas Biomedical Research Institute, Southwest National Primate Research Center, San Antonio, Texas 78227, United States</nlm:aff></affiliation></author></analytic><series><title level="j">Brain, Behavior, and Immunity</title><idno type="ISSN">0889-1591</idno><idno type="eISSN">1090-2139</idno><imprint><date when="2020">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Fu, B" uniqKey="Fu B">B. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Brain Behav Immun</journal-id><journal-id journal-id-type="iso-abbrev">Brain Behav. Immun</journal-id><journal-title-group><journal-title>Brain, Behavior, and Immunity</journal-title></journal-title-group><issn pub-type="ppub">0889-1591</issn><issn pub-type="epub">1090-2139</issn><publisher><publisher-name>Elsevier Inc.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmc">7187842</article-id><article-id pub-id-type="publisher-id">S0889-1591(20)30707-8</article-id><article-id pub-id-type="doi">10.1016/j.bbi.2020.04.079</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>SARS-CoV2 induced respiratory distress: Can Cannabinoids be added to anti-viral therapies to reduce lung inflammation?</article-title></title-group><contrib-group><contrib contrib-type="author" id="au005"><name><surname>Byrareddy</surname><given-names>Siddappa N.</given-names></name><xref rid="af005" ref-type="aff">a</xref></contrib><contrib contrib-type="author" id="au010"><name><surname>Mohan</surname><given-names>Mahesh</given-names></name><email>mmohan@txbiomed.org</email><xref rid="af010" ref-type="aff">b</xref><xref rid="cor1" ref-type="corresp">⁎</xref></contrib><aff id="af005"><label>a</label>Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska 68198, United States</aff><aff id="af010"><label>b</label>Texas Biomedical Research Institute, Southwest National Primate Research Center, San Antonio, Texas 78227, United States</aff></contrib-group><author-notes><corresp id="cor1"><label>⁎</label>Corresponding author at: Texas Biomedical Research Institute, Southwest National Primate Research Center, 8715 West Military Road, San Antonio, Texas 78258, United States <email>mmohan@txbiomed.org</email></corresp></author-notes><pub-date pub-type="pmc-release"><day>28</day><month>4</month><year>2020</year></pub-date><pmc-comment> PMC Release delay is 0 months and 0 days and was based on .</pmc-comment>
<pub-date pub-type="epub"><day>28</day><month>4</month><year>2020</year></pub-date><history><date date-type="received"><day>27</day><month>4</month><year>2020</year></date><date date-type="accepted"><day>27</day><month>4</month><year>2020</year></date></history><permissions><copyright-statement>© 2020 Elsevier Inc. All rights reserved.</copyright-statement><copyright-year>2020</copyright-year><copyright-holder></copyright-holder><license><license-p>Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.</license-p></license></permissions><kwd-group id="kg005"><title>Keywords</title><kwd>SARS-CoV2</kwd><kwd>rhesus macaque</kwd><kwd>cannabinoids</kwd><kwd>inflammation</kwd><kwd>cytokine</kwd><kwd>lung</kwd></kwd-group></article-meta></front><body><p id="p0005">Coronavirus disease-2019 (COVID-19), caused by Severe Acute Respiratory Syndrome coronoavirus-2 (SARS-CoV2) has emerged as a global pandemic, which was first reported in Wuhan, China. Recent reports have suggested that acute infection is associated with a cytokine superstorm, which contributes to the symptoms of fever, cough, muscle pain and in severe cases bilateral interstitial pneumonia characterized by ground glass opacity and focal chest infiltrates that can be visualized on computerized tomography scans (<xref rid="b0030" ref-type="bibr">Rothan and Byrareddy, 2020</xref>). Currently, there are no effective antiviral drugs or vaccines against SARS-CoV2. In the recent issue of BBI, Zhang et al. (<xref rid="b0050" ref-type="bibr">Zhang et al., 2020</xref>) thoroughly summarized the current status of potential therapeutic strategies for COVID-19. One of them, anti-IL6 receptor (Tocilizumab) antibody, resulted in clearance of lung consolidation and recovery in 90% of the 21 treated patients (<xref rid="b0005" ref-type="bibr">Fu et al., 2020</xref>). Although promising, it has also produced adverse effects like pancreatitis and hypertriglyceridemia (<xref rid="b0015" ref-type="bibr">Morrison et al., 2020</xref>), which make it imperative to explore effective alternative anti-inflammatory strategies. Here, we intend to highlight the potential effects of cannabinoids, in particular, the non-psychotropic cannabidiol (CBD), that has shown beneficial anti-inflammatory effects in pre-clinical models of various chronic inflammatory diseases and is FDA approved for seizure reduction in children with intractable epilepsy (<xref rid="b0020" ref-type="bibr">Nichols and Kaplan, 2020</xref>).</p><p id="p0010">Similar to Δ<sup>9</sup>-tetrahydrocannabinol (Δ<sup>9</sup>-THC), the most studied cannabinoid, CBD decreased lung inflammation in a murine model of acute lung injury potentially through the inhibition of proinflammatory cytokine production by immune cells and suppressing exuberant immune responses (<xref rid="b0035" ref-type="bibr">Vuolo et al., 2019</xref>). CBD can inhibit the production of proinflammatory cytokines like interleukin (IL)-2, IL-6, IL-1α and β, interferon gamma, inducible protein-10, monocyte chemoattractant protein-1, macrophage inflammatory protein-1α, and tumor necrosis factor-α (<xref rid="b0020" ref-type="bibr">Nichols and Kaplan, 2020</xref>) (<xref rid="f0005" ref-type="fig">Figure 1</xref>) that have been associated with SARS-CoV2 induced multi-organ pathology and mortality. In a murine model of chronic asthma, CBD reduced proinflammatory cytokine production, airway inflammation and fibrosis (<xref rid="b0035" ref-type="bibr">Vuolo et al., 2019</xref>). Moreover, CBD can effectively inhibit the JAK-STAT pathway including the production and action of type I interferons without leading to addiction, alterations in heart rate or blood pressure and adverse effects on the gastrointestinal tract and cognition (<xref rid="b0020" ref-type="bibr">Nichols and Kaplan, 2020</xref>). In simian immunodeficiency virus (SIV)-infected rhesus macaques (RMs), we reported THC mediated attenuation of IFN stimulated gene expression in the intestine (<xref rid="b0010" ref-type="bibr">Kumar et al., 2019</xref>). Similar to CBD, chronic THC administration blocked inflammation induced fibrosis in lymph nodes of chronically SIV-infected RMs (<xref rid="b0010" ref-type="bibr">Kumar et al., 2019</xref>). Unlike THC, CBD has a high margin of safety and is well tolerated pharmacologically even after treatments of up to 1500 mg/day for two weeks in both animals and humans (<xref rid="b0020" ref-type="bibr">Nichols and Kaplan, 2020</xref>), which suggests its feasibility to reduce SARS-CoV2 induced lung inflammation/pathology and disease severity.<fig id="f0005"><label>Figure 1</label><caption><p>Potential mechanisms associated with cannabinoid mediated suppression of SARS-CoV-2 induced lung inflammation and fibrosis. ROS- Reactive oxygen species, IL- Interleukin; IFN- Interferon; MIP- Macrophage inhibitory protein; MCP- Monocyte chemotactic protein; ER-Endoplasmic reticulum.</p></caption><graphic xlink:href="gr1_lrg"></graphic></fig></p><p id="p0015">The many uncertainties associated with the COVID-19 pandemic such as status of the economy, employment and loss of connection can fuel depression, fear and anxiety. CBD has shown promise as an alternative therapy for the clinical management of anxiety disorders (<xref rid="b0020" ref-type="bibr">Nichols and Kaplan, 2020</xref>). Based on its anxiolytic and anti-depressant properties, it has been suggested CBD could be used to improve the mental and somatic health of patients suffering from anxiety and emotional stress after recovering from Ebola disease (<xref rid="b0025" ref-type="bibr">Reznik et al., 2016</xref>). Like Ebola, patients recovering from COVID-19 may experience various psychological and social stressors that may be triggered by residual chronic inflammation and autoimmune reactions. Therefore, randomized clinical trials to test the efficacy of CBD on alleviating anxiety and fear associated with COVID-19 infection and its consequences on people’s physical, social and psychological well-being may be beneficial in the future. Additionally, severely ill COVID-19 patients exhibited neurological symptoms like cerebrovascular disease, headache and disturbed consciousness (Reviewed in (<xref rid="b0045" ref-type="bibr">Wu et al., 2020</xref>)). Brain edema, neuronal degeneration and presence of SARS-CoV2 in the cerebrospinal fluid (CSF) were confirmed at autopsy (<xref rid="b0045" ref-type="bibr">Wu et al., 2020</xref>). Therefore, longitudinal CSF sampling using non-human primate (NHP) studies may help clarify whether and when SARS-CoV2 invades the brain, and if this happens, does it result in neuroinflammation and more importantly, whether cannabinoids can modulate these events (<xref rid="b0010" ref-type="bibr">Kumar et al., 2019</xref>).</p><p id="p0020">Being a negative allosteric modulator of the cannabinoid receptor-1, CBD can counter the psychotropic effects of THC when co-administered with THC (<xref rid="b0020" ref-type="bibr">Nichols and Kaplan, 2020</xref>). Although, Remdesivir reduced the mortality rate of seriously ill COVID-19 patients needing invasive ventilation (<xref rid="b0050" ref-type="bibr">Zhang et al., 2020</xref>), similar studies in rhesus macaques revealed minimal subpleural inflammatory cellular infiltrates in the lungs of clinically recovered Remdesivir treated RMs at necropsy (<xref rid="b0040" ref-type="bibr">Williamson et al., 2020</xref>). This suggests persistence of inflammation and may partly explain the 20-30% reduction in lung function in COVID-19 patients after recovery, which if left unresolved may lead to pulmonary fibrosis. Therefore, these findings support the investigation of cannabinoids as a plausible option to be added as an adjunct to Remdesivir or any new antivirals on SARS-CoV2 induced lung inflammation.</p><p id="p0025">This work was supported by the National Institutes of Health Award Numbers R01DA042524, R01DA050169 and R56DE026930 to MM, and OD011104 formerly RR00164. 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