HDL proteome remodeling associates with COVID-19 severity
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Citações na Scopus
23
Tipo de produção
article
Data de publicação
2021
Título da Revista
ISSN da Revista
Título do Volume
Editora
ELSEVIER SCIENCE INC
Autores
SOUZA JUNIOR, Douglas Ricardo
SILVA, Amanda Ribeiro Martins
ROSA-FERNANDES, Livia
REIS, Lorenna Rocha
ALEXANDRIA, Gabrielly
BHOSALE, Santosh D.
Citação
JOURNAL OF CLINICAL LIPIDOLOGY, v.15, n.6, p.796-804, 2021
Resumo
Background: Besides the well-accepted role in lipid metabolism, high-density lipoprotein (HDL) also seems to participate in host immune response against infectious diseases. Objective : We used a quantitative proteomic approach to test the hypothesis that alterations in HDL proteome associate with severity of Coronavirus disease 2019 (COVID-19). Methods: Based on clinical criteria, subjects (n = 41) diagnosed with COVID-19 were divided into two groups: a group of subjects presenting mild symptoms and a second group displaying severe symptoms and requiring hospitalization. Using a proteomic approach, we quantified the levels of 29 proteins in HDL particles derived from these subjects. Results: We showed that the levels of serum amyloid A 1 and 2 (SAA1 and SAA2, respectively), pulmonary surfactant-associated protein B (SFTPB), apolipoprotein F (APOF), and inter-alpha-trypsin inhibitor heavy chain H4 (ITIH4) were increased by more than 50% in hospitalized patients, independently of sex, HDL-C or triglycerides when comparing with subjects presenting only mild symptoms. Altered HDL proteins were able to classify COVID-19 subjects according to the severity of the disease (error rate 4.9%). Moreover, apolipoprotein M (APOM) in HDL was inversely associated with odds of death due to COVID-19 complications (odds ratio [OR] per 1-SD increase in APOM was 0.27, with 95% confidence interval [CI] of 0.07 to 0.72, P = 0.007). Conclusion: Our results point to a profound inflammatory remodeling of HDL proteome tracking with severity of COVID-19 infection. They also raise the possibility that HDL particles could play an important role in infectious diseases.
Palavras-chave
Quantitative proteomics, Infection, HDL, COVID-19
Referências
- Banfi C, 2016, INT J CARDIOL, V221, P456, DOI 10.1016/j.ijcard.2016.07.003
- Begue F, 2021, SCI REP-UK, V11, DOI 10.1038/s41598-021-81638-1
- Birner-Gruenberger R, 2014, PROG LIPID RES, V56, P36, DOI 10.1016/j.plipres.2014.07.003
- Brodin P, 2021, NAT MED, V27, P28, DOI 10.1038/s41591-020-01202-8
- Carr SA, 2014, MOL CELL PROTEOMICS, V13, P907, DOI 10.1074/mcp.M113.036095
- Cartier A, 2019, SCIENCE, V366, P323, DOI 10.1126/science.aar5551
- Chien JY, 2005, CRIT CARE MED, V33, P1688, DOI 10.1097/01.CCM.0000171183.79525.6B
- Dickinson A, 2020, PLOS ONE, V15, DOI 10.1371/journal.pone.0233974
- Doyle IR, 1997, AM J RESP CRIT CARE, V156, P1217, DOI 10.1164/ajrccm.156.4.9603061
- Dupont A, 2021, ARTERIOSCL THROM VAS, V41, P1760, DOI 10.1161/ATVBAHA.120.315595
- Fan JL, 2020, METABOLISM, V107, DOI 10.1016/j.metabol.2020.154243
- Fan YW, 2020, INT J BIOCHEM CELL B, V126, DOI 10.1016/j.biocel.2020.105819
- Frej C, 2017, ARTERIOSCL THROM VAS, V37, P1194, DOI 10.1161/ATVBAHA.117.309275
- Galvani S, 2015, SCI SIGNAL, V8, DOI 10.1126/scisignal.aaa2581
- Gebhard C, 2020, BIOL SEX DIFFER, V11, DOI 10.1186/s13293-020-00304-9
- Gordon SM, 2013, MOL CELL PROTEOMICS, V12, P3123, DOI 10.1074/mcp.M113.028134
- Gordon SM, 2013, DIABETES, V62, P2958, DOI 10.2337/db12-1753
- Han CY, 2016, J CLIN INVEST, V126, P796, DOI 10.1172/JCI86401
- Heinecke JW, 2020, ARTERIOSCL THROM VAS, V40, P5, DOI 10.1161/ATVBAHA.119.313651
- Holzer M, 2012, J LIPID RES, V53, P1618, DOI 10.1194/jlr.M027367
- Hu XZ, 2020, CLIN CHIM ACTA, V510, P105, DOI 10.1016/j.cca.2020.07.015
- Jin YF, 2020, SIGNAL TRANSDUCT TAR, V5, DOI 10.1038/s41392-020-00454-7
- Kaysen GA, 2018, J LIPID RES, V59, P1519, DOI [10.1194/jlr.P084277, 10.1194/jlr.p084277]
- Lagor WR, 2014, ATHEROSCLEROSIS, V233, P234, DOI 10.1016/j.atherosclerosis.2013.12.043
- Lekkou A, 2014, J CRIT CARE, V29, P723, DOI 10.1016/j.jcrc.2014.04.018
- Li H, 2020, J INFECTION, V80, P646, DOI 10.1016/j.jinf.2020.03.035
- Liu Y, 2020, CURR OPIN LIPIDOL, V31, P194, DOI 10.1097/MOL.0000000000000688
- Madsen CM, 2018, EUR HEART J, V39, P1181, DOI 10.1093/eurheartj/ehx665
- Masana L, 2021, SCI REP-UK, V11, DOI 10.1038/s41598-021-86747-5
- Melchior JT, 2017, J LIPID RES, V58, P1374, DOI 10.1194/jlr.M075382
- Pestka S, 2004, IMMUNOL REV, V202, P8, DOI 10.1111/j.0105-2896.2004.00204.x
- Pirillo A, 2015, HANDB EXP PHARMACOL, V224, P483, DOI 10.1007/978-3-319-09665-0_15
- Ronsein GE, 2016, MOL CELL PROTEOMICS, V15, P1083, DOI 10.1074/mcp.M115.054528
- Ronsein GE, 2015, J PROTEOMICS, V113, P388, DOI 10.1016/j.jprot.2014.10.017
- Ruiz M, 2017, ARTERIOSCL THROM VAS, V37, P118, DOI 10.1161/ATVBAHA.116.308435
- Schuchardt M, 2019, SCI REP-UK, V9, DOI 10.1038/s41598-019-39846-3
- Shah AS, 2013, J LIPID RES, V54, P2575, DOI 10.1194/jlr.R035725
- Silva ARM, 2020, J PROTEOME RES, V19, P248, DOI 10.1021/acs.jproteome.9b00511
- Singh SA, 2021, JCI INSIGHT, V6, DOI 10.1172/jci.insight.143526
- Tall AR, 2015, NAT REV IMMUNOL, V15, P104, DOI 10.1038/nri3793
- Tanaka S, 2020, PLOS ONE, V15, DOI 10.1371/journal.pone.0239573
- Tolle M, 2012, CARDIOVASC RES, V94, P154, DOI 10.1093/cvr/cvs089
- Trieb M, 2020, J HEPATOL, V73, P113, DOI 10.1016/j.jhep.2020.01.026
- Trinder M, 2021, CIRCULATION, V143, P921, DOI 10.1161/CIRCULATIONAHA.120.048568
- Trinder M, 2020, ARTERIOSCL THROM VAS, V40, P267, DOI 10.1161/ATVBAHA.119.313381
- Vaisar T, 2015, J LIPID RES, V56, P1519, DOI 10.1194/jlr.M059089
- Vidova V, 2017, ANAL CHIM ACTA, V964, P7, DOI 10.1016/j.aca.2017.01.059
- Wang D, 2020, BMC INFECT DIS, V20, DOI 10.1186/s12879-020-05242-w
- Watanabe J, 2012, ARTHRITIS RHEUM-US, V64, P1828, DOI 10.1002/art.34363
- Weichhart T, 2012, J AM SOC NEPHROL, V23, P934, DOI 10.1681/ASN.2011070668
- Wiersinga WJ, 2020, JAMA-J AM MED ASSOC, V324, P782, DOI 10.1001/jama.2020.12839
- Zewinger S, 2015, EUR HEART J, V36, P3007, DOI 10.1093/eurheartj/ehv352