Endogenous and Therapeutic 25-Hydroxycholesterols May Worsen Early SARS-CoV-2 Pathogenesis in Mice

Oxysterols (i.e., oxidized cholesterol species) have complex roles in biology. 25-Hydroxycholesterol (25HC), a product of the activity of cholesterol-25-hydroxylase (CH25H) on cholesterol, has recently been shown to be broadly antiviral, suggesting therapeutic potential against severe acute respirat...

Full description

Saved in:
Bibliographic Details
Published inAmerican journal of respiratory cell and molecular biology Vol. 69; no. 6; pp. 638 - 648
Main Authors Fessler, Michael B, Madenspacher, Jennifer H, Baker, Paul J, Hilligan, Kerry L, Bohrer, Andrea C, Castro, Ehydel, Meacham, Julie, Chen, Shih-Heng, Johnson, Reed F, McDonald, Jeffrey G, Martin, Negin P, Tucker, Charles J, Mahapatra, Debabrata, Cesta, Mark, Mayer-Barber, Katrin D
Format Journal Article
LanguageEnglish
Published United States American Thoracic Society 01.12.2023
Subjects
Online AccessGet full text

Cover

Loading…
Abstract Oxysterols (i.e., oxidized cholesterol species) have complex roles in biology. 25-Hydroxycholesterol (25HC), a product of the activity of cholesterol-25-hydroxylase (CH25H) on cholesterol, has recently been shown to be broadly antiviral, suggesting therapeutic potential against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). However, 25HC can also amplify inflammation and be converted by CYP7B1 (cytochrome P450 family 7 subfamily B member 1) to 7α,25-dihydroxycholesterol, a lipid with chemoattractant activity, via the G protein-coupled receptor EBI2 (Epstein-Barr virus-induced gene 2)/GPR183 (G protein-coupled receptor 183). Here, using studies and two different murine models of SARS-CoV-2 infection, we investigate the effects of these two oxysterols on SARS-CoV-2 pneumonia. We show that although 25HC and enantiomeric-25HC are antiviral against human endemic coronavirus-229E, they did not inhibit SARS-CoV-2; nor did supplemental 25HC reduce pulmonary SARS-CoV-2 titers in the K18-human ACE2 (angiotensin-converting enzyme 2) mouse model . Treatment with 25HC also did not alter immune cell influx into the airway, airspace cytokines, lung pathology, weight loss, symptoms, or survival but was associated with increased airspace albumin, an indicator of microvascular injury, and increased plasma proinflammatory cytokines. Conversely, mice treated with the EBI2/GPR183 inhibitor NIBR189 displayed a modest increase in lung viral load only at late time points but no change in weight loss. Consistent with these findings, although and 25HC were upregulated in the lungs of SARS-CoV-2-infected wild-type mice, lung viral titers and weight loss in and mice infected with the β variant were similar to those in control animals. Taken together, endogenous 25HCs do not significantly regulate early SARS-CoV-2 replication or pathogenesis, and supplemental 25HC may have proinjury rather than therapeutic effects in SARS-CoV-2 pneumonia.
AbstractList Oxysterols (i.e., oxidized cholesterol species) have complex roles in biology. 25-Hydroxycholesterol (25HC), a product of the activity of cholesterol-25-hydroxylase (CH25H) on cholesterol, has recently been shown to be broadly antiviral, suggesting therapeutic potential against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). However, 25HC can also amplify inflammation and be converted by CYP7B1 (cytochrome P450 family 7 subfamily B member 1) to 7α,25-dihydroxycholesterol, a lipid with chemoattractant activity, via the G protein-coupled receptor EBI2 (Epstein-Barr virus-induced gene 2)/GPR183 (G protein-coupled receptor 183). Here, using in vitro studies and two different murine models of SARS-CoV-2 infection, we investigate the effects of these two oxysterols on SARS-CoV-2 pneumonia. We show that although 25HC and enantiomeric-25HC are antiviral in vitro against human endemic coronavirus-229E, they did not inhibit SARS-CoV-2; nor did supplemental 25HC reduce pulmonary SARS-CoV-2 titers in the K18-human ACE2 (angiotensin-converting enzyme 2) mouse model in vivo. Treatment with 25HC also did not alter immune cell influx into the airway, airspace cytokines, lung pathology, weight loss, symptoms, or survival but was associated with increased airspace albumin, an indicator of microvascular injury, and increased plasma proinflammatory cytokines. Conversely, mice treated with the EBI2/GPR183 inhibitor NIBR189 displayed a modest increase in lung viral load only at late time points but no change in weight loss. Consistent with these findings, although Ch25h and 25HC were upregulated in the lungs of SARS-CoV-2-infected wild-type mice, lung viral titers and weight loss in Ch25h-/- and Gpr183-/- mice infected with the β variant were similar to those in control animals. Taken together, endogenous 25HCs do not significantly regulate early SARS-CoV-2 replication or pathogenesis, and supplemental 25HC may have proinjury rather than therapeutic effects in SARS-CoV-2 pneumonia.
Fessler et al present a study which investigates the effects of two oxysterols on SARS-CoV-2 pneumonia using in vitro studies and two different murine models of SARS-CoV-2 infection. They show that although 25HC and enantiomeric-25HC are antiviral in vitro against human endemic coronavirus-229E, they did not inhibit SARS-CoV-2; nor did supplemental 25HC reduce pulmonary SARS-CoV-2 titers in the K18-human ACE2 (angiotensin-converting enzyme 2) mouse model in vivo. They note that endogenous 25HCs do not significantly regulate early SARS-CoV-2 replication or pathogenesis, and supplemental 25HC may have proinjury rather than therapeutic effects in SARS-CoV-2 pneumonia.
Oxysterols (i.e., oxidized cholesterol species) have complex roles in biology. 25-Hydroxycholesterol (25HC), a product of the activity of cholesterol-25-hydroxylase (CH25H) on cholesterol, has recently been shown to be broadly antiviral, suggesting therapeutic potential against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). However, 25HC can also amplify inflammation and be converted by CYP7B1 (cytochrome P450 family 7 subfamily B member 1) to 7α,25-dihydroxycholesterol, a lipid with chemoattractant activity, via the G protein-coupled receptor EBI2 (Epstein-Barr virus-induced gene 2)/GPR183 (G protein-coupled receptor 183). Here, using studies and two different murine models of SARS-CoV-2 infection, we investigate the effects of these two oxysterols on SARS-CoV-2 pneumonia. We show that although 25HC and enantiomeric-25HC are antiviral against human endemic coronavirus-229E, they did not inhibit SARS-CoV-2; nor did supplemental 25HC reduce pulmonary SARS-CoV-2 titers in the K18-human ACE2 (angiotensin-converting enzyme 2) mouse model . Treatment with 25HC also did not alter immune cell influx into the airway, airspace cytokines, lung pathology, weight loss, symptoms, or survival but was associated with increased airspace albumin, an indicator of microvascular injury, and increased plasma proinflammatory cytokines. Conversely, mice treated with the EBI2/GPR183 inhibitor NIBR189 displayed a modest increase in lung viral load only at late time points but no change in weight loss. Consistent with these findings, although and 25HC were upregulated in the lungs of SARS-CoV-2-infected wild-type mice, lung viral titers and weight loss in and mice infected with the β variant were similar to those in control animals. Taken together, endogenous 25HCs do not significantly regulate early SARS-CoV-2 replication or pathogenesis, and supplemental 25HC may have proinjury rather than therapeutic effects in SARS-CoV-2 pneumonia.
Author Fessler, Michael B
Tucker, Charles J
Cesta, Mark
Meacham, Julie
Castro, Ehydel
Hilligan, Kerry L
Baker, Paul J
Bohrer, Andrea C
McDonald, Jeffrey G
Mayer-Barber, Katrin D
Martin, Negin P
Mahapatra, Debabrata
Johnson, Reed F
Madenspacher, Jennifer H
Chen, Shih-Heng
Author_xml – sequence: 1
  givenname: Michael B
  surname: Fessler
  fullname: Fessler, Michael B
  organization: Immunity, Inflammation and Disease Laboratory
– sequence: 2
  givenname: Jennifer H
  surname: Madenspacher
  fullname: Madenspacher, Jennifer H
  organization: Immunity, Inflammation and Disease Laboratory
– sequence: 3
  givenname: Paul J
  surname: Baker
  fullname: Baker, Paul J
  organization: Inflammation and Innate Immunity Unit
– sequence: 4
  givenname: Kerry L
  surname: Hilligan
  fullname: Hilligan, Kerry L
  organization: Immunobiology Section, and
– sequence: 5
  givenname: Andrea C
  surname: Bohrer
  fullname: Bohrer, Andrea C
  organization: Inflammation and Innate Immunity Unit
– sequence: 6
  givenname: Ehydel
  surname: Castro
  fullname: Castro, Ehydel
  organization: Inflammation and Innate Immunity Unit
– sequence: 7
  givenname: Julie
  surname: Meacham
  fullname: Meacham, Julie
  organization: Immunity, Inflammation and Disease Laboratory
– sequence: 8
  givenname: Shih-Heng
  surname: Chen
  fullname: Chen, Shih-Heng
  organization: Viral Vector Core Facility, Neurobiology Laboratory
– sequence: 9
  givenname: Reed F
  surname: Johnson
  fullname: Johnson, Reed F
  organization: SARS-CoV-2 Virology Core, Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland
– sequence: 10
  givenname: Jeffrey G
  surname: McDonald
  fullname: McDonald, Jeffrey G
  organization: Center for Human Nutrition, University of Texas Southwestern Medical Center, Dallas, Texas; and
– sequence: 11
  givenname: Negin P
  surname: Martin
  fullname: Martin, Negin P
  organization: Viral Vector Core Facility, Neurobiology Laboratory
– sequence: 12
  givenname: Charles J
  surname: Tucker
  fullname: Tucker, Charles J
  organization: Fluorescence Microscopy and Imaging Center, Signal Transduction Laboratory, and
– sequence: 13
  givenname: Debabrata
  surname: Mahapatra
  fullname: Mahapatra, Debabrata
  organization: Integrated Laboratory Systems, LLC, Research Triangle Park, North Carolina
– sequence: 14
  givenname: Mark
  surname: Cesta
  fullname: Cesta, Mark
  organization: Division of the National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina
– sequence: 15
  givenname: Katrin D
  surname: Mayer-Barber
  fullname: Mayer-Barber, Katrin D
  organization: Inflammation and Innate Immunity Unit
BackLink https://www.ncbi.nlm.nih.gov/pubmed/37578898$$D View this record in MEDLINE/PubMed
BookMark eNpdkD1PHDEQhq2IiK_Qp0KWaGhMxvb61i7R6QiRQCAgUFpe75hbtGcf9q3E_vvs6UiKVDPF876aeY7IXkwRCfnO4YLzmfqR_aq5ECAkA4D6bv6FHHIlFauMNnvTDlXFuKrMATkq5Q2AC835PjmQtaq1NvqQNIvYpleMaSjUxZY-LTG7NQ6bzlOh2PXY5vQx-mXqsWwwp77QWzfSl5QLRrpwuR_p4-XDI5unZybovdsst3VYukK7SG87j9_I1-D6gief85j8vlo8za_Zzd3PX_PLG-blzGyY0wbCzKHjlRNokEspUBkhQ214EDMvfOOU0iAUhCYYUYFvPdQBVaNDo-UxOd_1rnN6H6Zz7aorHvveRZzes0IrziteGTmhZ_-hb2nIcbrOCgMglYFaTBTsKJ9TKRmDXedu5fJoOditf7v1b7f-7c7_FDn9LB6aFbb_An-Fyz-POoJ_
CitedBy_id crossref_primary_10_1165_rcmb_2023_0301ED
Cites_doi 10.1038/s41422-020-00398-1
10.1038/nature10280
10.1513/AnnalsATS.201702-136AW
10.1016/j.immuni.2019.04.001
10.1016/j.jaut.2014.10.001
10.1164/rccm.201608-1580OC
10.3390/ijms222111869
10.1172/jci.insight.123971
10.1073/pnas.1404271111
10.1152/ajpendo.00218.2016
10.1007/s00011-013-0660-x
10.1016/j.celrep.2022.111144
10.1016/0013-9351(76)90107-9
10.1093/infdis/jiac102
10.1016/j.it.2016.09.001
10.1096/fj.202002555R
10.1007/s11882-015-0548-7
10.1038/s41590-020-0778-2
10.1016/j.molmet.2020.100983
10.15252/embj.2020106057
10.1074/jbc.M113.519637
10.7554/eLife.83534
10.1016/j.nantod.2021.101149
10.1016/j.immuni.2012.11.004
10.1016/j.chom.2014.10.003
10.15252/emmm.201708349
10.1194/jlr.M084558
10.1165/rcmb.2021-0531ST
10.1073/pnas.2012197117
10.1016/j.cell.2017.09.029
10.1016/j.immuni.2012.11.005
10.1016/j.antiviral.2022.105343
10.1111/j.1440-1843.2012.02136.x
10.1038/nri3755
10.1016/j.vetmic.2019.03.004
10.1183/13993003.01306-2022
10.3390/v12060628
10.1016/S0076-6879(07)32006-5
10.1016/j.immuni.2017.02.012
10.1172/jci.insight.155448
10.1016/j.atherosclerosis.2009.04.001
10.1016/j.mam.2016.04.003
10.1038/nature10226
10.1073/pnas.0909142106
10.1161/CIRCRESAHA.121.318902
10.1016/j.vetmic.2019.02.035
10.1073/pnas.2109744118
10.1513/AnnalsATS.201703-263WS
ContentType Journal Article
Copyright Copyright American Thoracic Society Dec 2023
Copyright_xml – notice: Copyright American Thoracic Society Dec 2023
DBID CGR
CUY
CVF
ECM
EIF
NPM
AAYXX
CITATION
7T5
7TM
7TO
H94
K9.
7X8
DOI 10.1165/rcmb.2023-0007OC
DatabaseName Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
CrossRef
Immunology Abstracts
Nucleic Acids Abstracts
Oncogenes and Growth Factors Abstracts
AIDS and Cancer Research Abstracts
ProQuest Health & Medical Complete (Alumni)
MEDLINE - Academic
DatabaseTitle MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
CrossRef
AIDS and Cancer Research Abstracts
ProQuest Health & Medical Complete (Alumni)
Immunology Abstracts
Oncogenes and Growth Factors Abstracts
Nucleic Acids Abstracts
MEDLINE - Academic
DatabaseTitleList MEDLINE - Academic
AIDS and Cancer Research Abstracts
MEDLINE
Database_xml – sequence: 1
  dbid: NPM
  name: PubMed
  url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 2
  dbid: EIF
  name: MEDLINE
  url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search
  sourceTypes: Index Database
DeliveryMethod fulltext_linktorsrc
Discipline Medicine
Anatomy & Physiology
EISSN 1535-4989
EndPage 648
ExternalDocumentID 10_1165_rcmb_2023_0007OC
37578898
Genre Journal Article
Research Support, N.I.H., Intramural
Research Support, N.I.H., Extramural
GrantInformation_xml – fundername: Intramural NIH HHS
  grantid: Z01 ES102005
– fundername: NIDDK NIH HHS
  grantid: P30 DK127984
– fundername: NHLBI NIH HHS
  grantid: P01 HL160487
– fundername: NHLBI NIH HHS
  grantid: 1P30DK127984
– fundername: NIAID NIH HHS
  grantid: R21 AI129303
– fundername: NIEHS NIH HHS
  grantid: ES103316
– fundername: NCATS NIH HHS
  grantid: UL1 TR003163
– fundername: NIEHS NIH HHS
  grantid: Z01 ES102005
– fundername: NIDDK NIH HHS
  grantid: 5P01HL160487
GroupedDBID ---
0R~
23M
2WC
3V.
53G
5GY
5RE
7X7
88A
88E
88I
8AF
8AO
8FE
8FH
8FI
8FJ
8R4
8R5
ABJNI
ABUWG
ACGFO
ACGFS
ACGOD
ACPRK
ADBBV
AENEX
AFFNX
AFKRA
AHMBA
ALIPV
ALMA_UNASSIGNED_HOLDINGS
AZQEC
BAWUL
BBNVY
BENPR
BES
BHPHI
BPHCQ
BVXVI
C45
CCPQU
CGR
CS3
CUY
CVF
DIK
DWQXO
E3Z
EBS
ECM
EIF
EJD
EMOBN
F3I
F5P
FRP
FYUFA
GNUQQ
GX1
H13
HCIFZ
HMCUK
HZ~
J5H
LK8
M0L
M1P
M2P
M2Q
M5~
M7P
NPM
O9-
OBH
OFXIZ
OK1
OVD
OVIDX
P2P
PQQKQ
PROAC
PSQYO
PZZ
Q2X
RWL
S0X
SJN
TAE
TEORI
THO
TR2
UKHRP
W8F
WOQ
YHG
ZGI
ZXP
AAYXX
CITATION
7T5
7TM
7TO
H94
K9.
7X8
ID FETCH-LOGICAL-c369t-a890f6aea14a2e9e1332e5923f791f26c2cba5580250fbf9240cdc07fe5b8fb83
ISSN 1044-1549
IngestDate Wed Dec 04 03:56:10 EST 2024
Thu Dec 05 15:26:12 EST 2024
Fri Dec 06 04:02:42 EST 2024
Sat Nov 02 12:07:15 EDT 2024
IsDoiOpenAccess false
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 6
Keywords cholesterol-25-hydroxylase
25-hydroxycholesterol
SARS-CoV-2
pneumonia
EBI2
Language English
LinkModel OpenURL
MergedId FETCHMERGED-LOGICAL-c369t-a890f6aea14a2e9e1332e5923f791f26c2cba5580250fbf9240cdc07fe5b8fb83
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
OpenAccessLink https://doi.org/10.1165/rcmb.2023-0007oc
PMID 37578898
PQID 2900359072
PQPubID 2031371
PageCount 11
ParticipantIDs proquest_miscellaneous_2851141493
proquest_journals_2900359072
crossref_primary_10_1165_rcmb_2023_0007OC
pubmed_primary_37578898
PublicationCentury 2000
PublicationDate 2023-12-00
20231201
PublicationDateYYYYMMDD 2023-12-01
PublicationDate_xml – month: 12
  year: 2023
  text: 2023-12-00
PublicationDecade 2020
PublicationPlace United States
PublicationPlace_xml – name: United States
– name: New York
PublicationTitle American journal of respiratory cell and molecular biology
PublicationTitleAlternate Am J Respir Cell Mol Biol
PublicationYear 2023
Publisher American Thoracic Society
Publisher_xml – sequence: 0
  name: American Thoracic Society
References 37672661 - Am J Respir Cell Mol Biol. 2023 Dec;69(6):610-611
36263064 - bioRxiv. 2022 Sep 13
bib36
bib37
bib34
bib35
bib32
bib33
bib30
bib31
bib29
bib27
bib28
Lizard G (bib40) 1996; 148
bib47
bib48
bib45
bib46
bib43
bib44
bib41
bib42
bib9
bib7
bib8
bib6
bib3
bib38
bib4
bib39
bib1
bib2
bib50
bib14
bib15
bib12
bib13
bib10
bib11
bib49
Madenspacher JH (bib5) 2020; 5
bib25
bib26
bib23
bib24
bib21
bib22
bib20
bib18
bib19
bib16
bib17
References_xml – ident: bib16
  doi: 10.1038/s41422-020-00398-1
– ident: bib27
  doi: 10.1038/nature10280
– ident: bib49
  doi: 10.1513/AnnalsATS.201702-136AW
– ident: bib19
  doi: 10.1016/j.immuni.2019.04.001
– ident: bib28
  doi: 10.1016/j.jaut.2014.10.001
– ident: bib12
  doi: 10.1164/rccm.201608-1580OC
– ident: bib13
  doi: 10.3390/ijms222111869
– ident: bib29
  doi: 10.1172/jci.insight.123971
– ident: bib10
  doi: 10.1073/pnas.1404271111
– ident: bib41
  doi: 10.1152/ajpendo.00218.2016
– volume: 5
  start-page: e137189
  year: 2020
  ident: bib5
  publication-title: JCI Insight
  contributor:
    fullname: Madenspacher JH
– ident: bib39
  doi: 10.1007/s00011-013-0660-x
– ident: bib6
  doi: 10.1016/j.celrep.2022.111144
– ident: bib45
  doi: 10.1016/0013-9351(76)90107-9
– ident: bib11
  doi: 10.1093/infdis/jiac102
– ident: bib31
  doi: 10.1016/j.it.2016.09.001
– ident: bib44
  doi: 10.1096/fj.202002555R
– ident: bib36
  doi: 10.1007/s11882-015-0548-7
– ident: bib24
  doi: 10.1038/s41590-020-0778-2
– ident: bib48
  doi: 10.1016/j.molmet.2020.100983
– ident: bib17
  doi: 10.15252/embj.2020106057
– ident: bib34
  doi: 10.1074/jbc.M113.519637
– ident: bib35
  doi: 10.7554/eLife.83534
– ident: bib46
  doi: 10.1016/j.nantod.2021.101149
– ident: bib1
  doi: 10.1016/j.immuni.2012.11.004
– ident: bib33
  doi: 10.1016/j.chom.2014.10.003
– ident: bib4
  doi: 10.15252/emmm.201708349
– ident: bib32
  doi: 10.1194/jlr.M084558
– ident: bib18
  doi: 10.1165/rcmb.2021-0531ST
– ident: bib15
  doi: 10.1073/pnas.2012197117
– ident: bib9
  doi: 10.1016/j.cell.2017.09.029
– volume: 148
  start-page: 1625
  year: 1996
  ident: bib40
  publication-title: Am J Pathol
  contributor:
    fullname: Lizard G
– ident: bib2
  doi: 10.1016/j.immuni.2012.11.005
– ident: bib23
  doi: 10.1016/j.antiviral.2022.105343
– ident: bib47
  doi: 10.1111/j.1440-1843.2012.02136.x
– ident: bib26
  doi: 10.1038/nri3755
– ident: bib30
  doi: 10.1016/j.vetmic.2019.03.004
– ident: bib38
  doi: 10.1183/13993003.01306-2022
– ident: bib14
  doi: 10.3390/v12060628
– ident: bib22
  doi: 10.1016/S0076-6879(07)32006-5
– ident: bib7
  doi: 10.1016/j.immuni.2017.02.012
– ident: bib42
  doi: 10.1172/jci.insight.155448
– ident: bib43
  doi: 10.1016/j.atherosclerosis.2009.04.001
– ident: bib3
  doi: 10.1016/j.mam.2016.04.003
– ident: bib37
  doi: 10.1038/nature10226
– ident: bib21
  doi: 10.1073/pnas.0909142106
– ident: bib25
  doi: 10.1161/CIRCRESAHA.121.318902
– ident: bib8
  doi: 10.1016/j.vetmic.2019.02.035
– ident: bib20
  doi: 10.1073/pnas.2109744118
– ident: bib50
  doi: 10.1513/AnnalsATS.201703-263WS
SSID ssj0012811
Score 2.4818044
Snippet Oxysterols (i.e., oxidized cholesterol species) have complex roles in biology. 25-Hydroxycholesterol (25HC), a product of the activity of...
Fessler et al present a study which investigates the effects of two oxysterols on SARS-CoV-2 pneumonia using in vitro studies and two different murine models...
SourceID proquest
crossref
pubmed
SourceType Aggregation Database
Index Database
StartPage 638
SubjectTerms ACE2
Angiotensin
Angiotensin-converting enzyme 2
Animal models
Animals
Antiviral Agents - pharmacology
Antiviral drugs
Cholesterol
Coronaviruses
COVID-19
Cytokines
Epstein-Barr Virus Infections
Herpesvirus 4, Human
Humans
Hydroxycholesterols - pharmacology
Mice
Pathogenesis
Peptidyl-dipeptidase A
Pneumonia
Receptors, G-Protein-Coupled
Rodents
SARS-CoV-2
Severe acute respiratory syndrome coronavirus 2
Side effects
Weight Loss
Title Endogenous and Therapeutic 25-Hydroxycholesterols May Worsen Early SARS-CoV-2 Pathogenesis in Mice
URI https://www.ncbi.nlm.nih.gov/pubmed/37578898
https://www.proquest.com/docview/2900359072
https://search.proquest.com/docview/2851141493
Volume 69
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1Rb9MwELbKJk17QWMDVhiTkRASqjwSO06Tx24qVEAntHWob5HjOjCJplPbPXR_hT_LnR032dgk4CWKEsmJ_H253PnO3xHyRptQJiqJWWggXI3AQWYKiMQmRsD_HeyiMpjRHZ7Gg4vo01iOW61fjaql62V-pG_u3VfyP6jCNcAVd8n-A7LrQeECnAO-cASE4fhXGPfLyawSWcX171G9l6rDJRusJlijgvbNyiHMfi46Q7XC9fGFKTtO2vi8d3bOTmbfGEe1_h84nEGNkssSK-pv1QmtkzsNtYl5I1OPOQD7HlPfcrdTSTzV_ia4tY4jVbl-3fR5qMACgnnzJPJlN_XuiWNVVYBgNWOdzhrgitF3t4772czhRb40lzK4aJSFGG9-JYtS11TI22fXyqXiYdPYxk4X5s-fQIx6GXM9zY_sU9APcgqZDU5cTS0pBOr5J64R9h3hbX_rEdlElUVszPBxvK4fwgxk6PPesXx_93HbZMsPcNvleSCOsf7MaIc8rgIR2nOsekJaptwle70SsJyu6FtqS4Mtertka1hVYOyRvOYcBaxpg3P0fs5R4Bx1nKOWc7TmHG1yjl6WFDn3lFx86I9OBqzq08G0iNMlU0kaFLEyKowUN6kJheBGQuRQdNOw4LHmOldSJuhuF3kBUxnoiQ66hZF5UuSJeEY2yllp9gmNJPwQBAQpGKdrYVSBYlFRV6VRkOuIt8k7P5XZlZNjyWwYG8sMEcgQgcwh0CYHfq6z6sNYZDy1opVBF4Z6vb4NJhW_EVUamL2MYxQShVEq2uS5w2j9MI_piwfvvCTbNbcPyMZyfm1egeO6zA_J5nH_9OvZoSXSb7PomhI
link.rule.ids 314,780,784,27924,27925,33744,33745
linkProvider Geneva Foundation for Medical Education and Research
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Endogenous+and+Therapeutic+25-Hydroxycholesterols+May+Worsen+Early+SARS-CoV-2+Pathogenesis+in+Mice&rft.jtitle=American+journal+of+respiratory+cell+and+molecular+biology&rft.au=Fessler%2C+Michael+B&rft.au=Madenspacher%2C+Jennifer+H&rft.au=Baker%2C+Paul+J&rft.au=Hilligan%2C+Kerry+L&rft.date=2023-12-01&rft.eissn=1535-4989&rft.volume=69&rft.issue=6&rft.spage=638&rft_id=info:doi/10.1165%2Frcmb.2023-0007OC&rft_id=info%3Apmid%2F37578898&rft.externalDocID=37578898
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1044-1549&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1044-1549&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1044-1549&client=summon