Association of polymorphisms in long pentraxin 3 and its plasma levels with COVID-19 severity
COVID-19 is an infectious respiratory disease caused by SARS-CoV-2. Pentraxin 3 (PTX3) is involved in the activation and regulation of the complement system, demonstrating an important role in the pathogenesis of COVID-19. The aim was to evaluate the association of single nucleotide polymorphisms in...
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| creator | Feitosa, Thiala Alves de Souza Sá, Mirela Vanessa Pereira, Vanessa Cardoso de Andrade Cavalcante, Marton Kaique Pereira, Valéria Rêgo Alves da Costa Armstrong, Anderson do Carmo, Rodrigo Feliciano |
| description | COVID-19 is an infectious respiratory disease caused by SARS-CoV-2. Pentraxin 3 (PTX3) is involved in the activation and regulation of the complement system, demonstrating an important role in the pathogenesis of COVID-19. The aim was to evaluate the association of single nucleotide polymorphisms in
PTX3
and its plasma levels with the severity of COVID-19. This is a retrospective cohort study, carried out between August 2020 and July 2021, including patients with confirmed COVID-19 hospitalized in 2 hospitals in the Northeast Region of Brazil. Polymorphisms in
PTX3
(rs1840680 and rs2305619) were determined by real-time PCR. PTX3 plasma levels were measured by ELISA. Serum levels of interleukin (IL)-6, IL-8, and IL-10 were determined by flow cytometry. A multivariate logistic regression model was used to identify parameters independently associated with COVID-19 severity.
P
values |
| doi_str_mv | 10.1007/s10238-022-00926-w |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9619017</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2730643735</sourcerecordid><originalsourceid>FETCH-LOGICAL-c474t-999f4ddf2fa8e096acb1c2175389cec85327e72062f4a68f9a53d6208e9080353</originalsourceid><addsrcrecordid>eNp9kcFu1DAQhi1ERUvhBTggS1y4hI7txLEvSNVCoVKlXoAbslzH2XXlxMGT7bJvX7Nb2tIDp_F4_vlnRh8hbxh8YADtCTLgQlXAeQWguaw2z8gRazSrdMPV80fvQ_IS8RqANUrAC3IopGCNYHBEfp4iJhfsHNJIU0-nFLdDytMq4IA0jDSmcUknP87Z_i6poHbsaJiRTtHiYGn0Nz4i3YR5RReXP84_VUxTLJ85zNtX5KC3Ef3ru3hMvp99_rb4Wl1cfjlfnF5Urm7rudJa93XX9by3yoOW1l0xx1nbCKWdd6oRvPUtB8n72krVa9uITnJQXoMC0Yhj8nHvO62vBt-53brRTDkMNm9NssH8WxnDyizTjdGSaWBtMXh_Z5DTr7XH2QwBnY_Rjj6t0fBWgKxFu5v17on0Oq3zWM4zXNU1k1pqVVR8r3I5IWbf3y_DwPyhZ_b0TKFndvTMpjS9fXzGfctfXEUg9gIspXHp88Ps_9jeAgsopdM</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2844169698</pqid></control><display><type>article</type><title>Association of polymorphisms in long pentraxin 3 and its plasma levels with COVID-19 severity</title><source>SpringerLink Journals - AutoHoldings</source><creator>Feitosa, Thiala Alves ; de Souza Sá, Mirela Vanessa ; Pereira, Vanessa Cardoso ; de Andrade Cavalcante, Marton Kaique ; Pereira, Valéria Rêgo Alves ; da Costa Armstrong, Anderson ; do Carmo, Rodrigo Feliciano</creator><creatorcontrib>Feitosa, Thiala Alves ; de Souza Sá, Mirela Vanessa ; Pereira, Vanessa Cardoso ; de Andrade Cavalcante, Marton Kaique ; Pereira, Valéria Rêgo Alves ; da Costa Armstrong, Anderson ; do Carmo, Rodrigo Feliciano</creatorcontrib><description>COVID-19 is an infectious respiratory disease caused by SARS-CoV-2. Pentraxin 3 (PTX3) is involved in the activation and regulation of the complement system, demonstrating an important role in the pathogenesis of COVID-19. The aim was to evaluate the association of single nucleotide polymorphisms in
PTX3
and its plasma levels with the severity of COVID-19. This is a retrospective cohort study, carried out between August 2020 and July 2021, including patients with confirmed COVID-19 hospitalized in 2 hospitals in the Northeast Region of Brazil. Polymorphisms in
PTX3
(rs1840680 and rs2305619) were determined by real-time PCR. PTX3 plasma levels were measured by ELISA. Serum levels of interleukin (IL)-6, IL-8, and IL-10 were determined by flow cytometry. A multivariate logistic regression model was used to identify parameters independently associated with COVID-19 severity.
P
values < 0.05 were considered significant. The study included 496 patients, classified as moderate (
n
= 267) and severe (
n
= 229) cases. The
PTX3
AA genotype (rs1840680) was independently associated with protection against severe COVID-19 (
P
= 0.037; odds ratio = 0.555). PTX3 plasma levels were significantly associated with COVID-19 severity and mortality (
P
< 0.05). PTX3 levels were significantly correlated with IL-6, IL-8, IL-10, C-reactive protein, total leukocytes, neutrophil-to-lymphocyte ratio, urea, creatinine, ferritin, length of hospital stay, and higher respiratory rate (
P
< 0.05). Our results revealed a protective effect of the
PTX3
AA genotype (rs1840680) on the development of severe forms of COVID-19. Additionally, PTX3 plasma levels were associated with the severity of COVID-19. The results of this study provide evidence of an important role of PTX3 in the immunopathology of COVID-19.</description><identifier>ISSN: 1591-9528</identifier><identifier>ISSN: 1591-8890</identifier><identifier>EISSN: 1591-9528</identifier><identifier>DOI: 10.1007/s10238-022-00926-w</identifier><identifier>PMID: 36315310</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>C-reactive protein ; Complement system ; COVID-19 ; Creatinine ; Enzyme-linked immunosorbent assay ; Ferritin ; Flow cytometry ; Hematology ; Interleukin 10 ; Interleukin 6 ; Interleukin 8 ; Internal Medicine ; Leukocytes (neutrophilic) ; Lymphocytes ; Medicine ; Medicine & Public Health ; Oncology ; Original ; Original Article ; Patients ; Pentraxins ; Plasma ; Plasma levels ; Respiration ; Respiratory diseases ; Serum levels ; Severe acute respiratory syndrome coronavirus 2 ; Single-nucleotide polymorphism</subject><ispartof>Clinical and experimental medicine, 2023-08, Vol.23 (4), p.1225-1233</ispartof><rights>The Author(s), under exclusive licence to Springer Nature Switzerland AG 2022. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2022. The Author(s), under exclusive licence to Springer Nature Switzerland AG.</rights><rights>The Author(s), under exclusive licence to Springer Nature Switzerland AG 2022, Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-999f4ddf2fa8e096acb1c2175389cec85327e72062f4a68f9a53d6208e9080353</citedby><cites>FETCH-LOGICAL-c474t-999f4ddf2fa8e096acb1c2175389cec85327e72062f4a68f9a53d6208e9080353</cites><orcidid>0000-0002-6637-8909 ; 0000-0001-9995-7352 ; 0000-0001-9601-6995 ; 0000-0002-7995-7360 ; 0000-0003-2586-7180 ; 0000-0003-3161-8922 ; 0000-0002-1030-9277</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10238-022-00926-w$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10238-022-00926-w$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36315310$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Feitosa, Thiala Alves</creatorcontrib><creatorcontrib>de Souza Sá, Mirela Vanessa</creatorcontrib><creatorcontrib>Pereira, Vanessa Cardoso</creatorcontrib><creatorcontrib>de Andrade Cavalcante, Marton Kaique</creatorcontrib><creatorcontrib>Pereira, Valéria Rêgo Alves</creatorcontrib><creatorcontrib>da Costa Armstrong, Anderson</creatorcontrib><creatorcontrib>do Carmo, Rodrigo Feliciano</creatorcontrib><title>Association of polymorphisms in long pentraxin 3 and its plasma levels with COVID-19 severity</title><title>Clinical and experimental medicine</title><addtitle>Clin Exp Med</addtitle><addtitle>Clin Exp Med</addtitle><description>COVID-19 is an infectious respiratory disease caused by SARS-CoV-2. Pentraxin 3 (PTX3) is involved in the activation and regulation of the complement system, demonstrating an important role in the pathogenesis of COVID-19. The aim was to evaluate the association of single nucleotide polymorphisms in
PTX3
and its plasma levels with the severity of COVID-19. This is a retrospective cohort study, carried out between August 2020 and July 2021, including patients with confirmed COVID-19 hospitalized in 2 hospitals in the Northeast Region of Brazil. Polymorphisms in
PTX3
(rs1840680 and rs2305619) were determined by real-time PCR. PTX3 plasma levels were measured by ELISA. Serum levels of interleukin (IL)-6, IL-8, and IL-10 were determined by flow cytometry. A multivariate logistic regression model was used to identify parameters independently associated with COVID-19 severity.
P
values < 0.05 were considered significant. The study included 496 patients, classified as moderate (
n
= 267) and severe (
n
= 229) cases. The
PTX3
AA genotype (rs1840680) was independently associated with protection against severe COVID-19 (
P
= 0.037; odds ratio = 0.555). PTX3 plasma levels were significantly associated with COVID-19 severity and mortality (
P
< 0.05). PTX3 levels were significantly correlated with IL-6, IL-8, IL-10, C-reactive protein, total leukocytes, neutrophil-to-lymphocyte ratio, urea, creatinine, ferritin, length of hospital stay, and higher respiratory rate (
P
< 0.05). Our results revealed a protective effect of the
PTX3
AA genotype (rs1840680) on the development of severe forms of COVID-19. Additionally, PTX3 plasma levels were associated with the severity of COVID-19. The results of this study provide evidence of an important role of PTX3 in the immunopathology of COVID-19.</description><subject>C-reactive protein</subject><subject>Complement system</subject><subject>COVID-19</subject><subject>Creatinine</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Ferritin</subject><subject>Flow cytometry</subject><subject>Hematology</subject><subject>Interleukin 10</subject><subject>Interleukin 6</subject><subject>Interleukin 8</subject><subject>Internal Medicine</subject><subject>Leukocytes (neutrophilic)</subject><subject>Lymphocytes</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Oncology</subject><subject>Original</subject><subject>Original Article</subject><subject>Patients</subject><subject>Pentraxins</subject><subject>Plasma</subject><subject>Plasma levels</subject><subject>Respiration</subject><subject>Respiratory diseases</subject><subject>Serum levels</subject><subject>Severe acute respiratory syndrome coronavirus 2</subject><subject>Single-nucleotide polymorphism</subject><issn>1591-9528</issn><issn>1591-8890</issn><issn>1591-9528</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><recordid>eNp9kcFu1DAQhi1ERUvhBTggS1y4hI7txLEvSNVCoVKlXoAbslzH2XXlxMGT7bJvX7Nb2tIDp_F4_vlnRh8hbxh8YADtCTLgQlXAeQWguaw2z8gRazSrdMPV80fvQ_IS8RqANUrAC3IopGCNYHBEfp4iJhfsHNJIU0-nFLdDytMq4IA0jDSmcUknP87Z_i6poHbsaJiRTtHiYGn0Nz4i3YR5RReXP84_VUxTLJ85zNtX5KC3Ef3ru3hMvp99_rb4Wl1cfjlfnF5Urm7rudJa93XX9by3yoOW1l0xx1nbCKWdd6oRvPUtB8n72krVa9uITnJQXoMC0Yhj8nHvO62vBt-53brRTDkMNm9NssH8WxnDyizTjdGSaWBtMXh_Z5DTr7XH2QwBnY_Rjj6t0fBWgKxFu5v17on0Oq3zWM4zXNU1k1pqVVR8r3I5IWbf3y_DwPyhZ_b0TKFndvTMpjS9fXzGfctfXEUg9gIspXHp88Ps_9jeAgsopdM</recordid><startdate>20230801</startdate><enddate>20230801</enddate><creator>Feitosa, Thiala Alves</creator><creator>de Souza Sá, Mirela Vanessa</creator><creator>Pereira, Vanessa Cardoso</creator><creator>de Andrade Cavalcante, Marton Kaique</creator><creator>Pereira, Valéria Rêgo Alves</creator><creator>da Costa Armstrong, Anderson</creator><creator>do Carmo, Rodrigo Feliciano</creator><general>Springer International Publishing</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-6637-8909</orcidid><orcidid>https://orcid.org/0000-0001-9995-7352</orcidid><orcidid>https://orcid.org/0000-0001-9601-6995</orcidid><orcidid>https://orcid.org/0000-0002-7995-7360</orcidid><orcidid>https://orcid.org/0000-0003-2586-7180</orcidid><orcidid>https://orcid.org/0000-0003-3161-8922</orcidid><orcidid>https://orcid.org/0000-0002-1030-9277</orcidid></search><sort><creationdate>20230801</creationdate><title>Association of polymorphisms in long pentraxin 3 and its plasma levels with COVID-19 severity</title><author>Feitosa, Thiala Alves ; de Souza Sá, Mirela Vanessa ; Pereira, Vanessa Cardoso ; de Andrade Cavalcante, Marton Kaique ; Pereira, Valéria Rêgo Alves ; da Costa Armstrong, Anderson ; do Carmo, Rodrigo Feliciano</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-999f4ddf2fa8e096acb1c2175389cec85327e72062f4a68f9a53d6208e9080353</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>C-reactive protein</topic><topic>Complement system</topic><topic>COVID-19</topic><topic>Creatinine</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Ferritin</topic><topic>Flow cytometry</topic><topic>Hematology</topic><topic>Interleukin 10</topic><topic>Interleukin 6</topic><topic>Interleukin 8</topic><topic>Internal Medicine</topic><topic>Leukocytes (neutrophilic)</topic><topic>Lymphocytes</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Oncology</topic><topic>Original</topic><topic>Original Article</topic><topic>Patients</topic><topic>Pentraxins</topic><topic>Plasma</topic><topic>Plasma levels</topic><topic>Respiration</topic><topic>Respiratory diseases</topic><topic>Serum levels</topic><topic>Severe acute respiratory syndrome coronavirus 2</topic><topic>Single-nucleotide polymorphism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Feitosa, Thiala Alves</creatorcontrib><creatorcontrib>de Souza Sá, Mirela Vanessa</creatorcontrib><creatorcontrib>Pereira, Vanessa Cardoso</creatorcontrib><creatorcontrib>de Andrade Cavalcante, Marton Kaique</creatorcontrib><creatorcontrib>Pereira, Valéria Rêgo Alves</creatorcontrib><creatorcontrib>da Costa Armstrong, Anderson</creatorcontrib><creatorcontrib>do Carmo, Rodrigo Feliciano</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Clinical and experimental medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Feitosa, Thiala Alves</au><au>de Souza Sá, Mirela Vanessa</au><au>Pereira, Vanessa Cardoso</au><au>de Andrade Cavalcante, Marton Kaique</au><au>Pereira, Valéria Rêgo Alves</au><au>da Costa Armstrong, Anderson</au><au>do Carmo, Rodrigo Feliciano</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Association of polymorphisms in long pentraxin 3 and its plasma levels with COVID-19 severity</atitle><jtitle>Clinical and experimental medicine</jtitle><stitle>Clin Exp Med</stitle><addtitle>Clin Exp Med</addtitle><date>2023-08-01</date><risdate>2023</risdate><volume>23</volume><issue>4</issue><spage>1225</spage><epage>1233</epage><pages>1225-1233</pages><issn>1591-9528</issn><issn>1591-8890</issn><eissn>1591-9528</eissn><abstract>COVID-19 is an infectious respiratory disease caused by SARS-CoV-2. Pentraxin 3 (PTX3) is involved in the activation and regulation of the complement system, demonstrating an important role in the pathogenesis of COVID-19. The aim was to evaluate the association of single nucleotide polymorphisms in
PTX3
and its plasma levels with the severity of COVID-19. This is a retrospective cohort study, carried out between August 2020 and July 2021, including patients with confirmed COVID-19 hospitalized in 2 hospitals in the Northeast Region of Brazil. Polymorphisms in
PTX3
(rs1840680 and rs2305619) were determined by real-time PCR. PTX3 plasma levels were measured by ELISA. Serum levels of interleukin (IL)-6, IL-8, and IL-10 were determined by flow cytometry. A multivariate logistic regression model was used to identify parameters independently associated with COVID-19 severity.
P
values < 0.05 were considered significant. The study included 496 patients, classified as moderate (
n
= 267) and severe (
n
= 229) cases. The
PTX3
AA genotype (rs1840680) was independently associated with protection against severe COVID-19 (
P
= 0.037; odds ratio = 0.555). PTX3 plasma levels were significantly associated with COVID-19 severity and mortality (
P
< 0.05). PTX3 levels were significantly correlated with IL-6, IL-8, IL-10, C-reactive protein, total leukocytes, neutrophil-to-lymphocyte ratio, urea, creatinine, ferritin, length of hospital stay, and higher respiratory rate (
P
< 0.05). Our results revealed a protective effect of the
PTX3
AA genotype (rs1840680) on the development of severe forms of COVID-19. Additionally, PTX3 plasma levels were associated with the severity of COVID-19. The results of this study provide evidence of an important role of PTX3 in the immunopathology of COVID-19.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>36315310</pmid><doi>10.1007/s10238-022-00926-w</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-6637-8909</orcidid><orcidid>https://orcid.org/0000-0001-9995-7352</orcidid><orcidid>https://orcid.org/0000-0001-9601-6995</orcidid><orcidid>https://orcid.org/0000-0002-7995-7360</orcidid><orcidid>https://orcid.org/0000-0003-2586-7180</orcidid><orcidid>https://orcid.org/0000-0003-3161-8922</orcidid><orcidid>https://orcid.org/0000-0002-1030-9277</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | C-reactive protein Complement system COVID-19 Creatinine Enzyme-linked immunosorbent assay Ferritin Flow cytometry Hematology Interleukin 10 Interleukin 6 Interleukin 8 Internal Medicine Leukocytes (neutrophilic) Lymphocytes Medicine Medicine & Public Health Oncology Original Original Article Patients Pentraxins Plasma Plasma levels Respiration Respiratory diseases Serum levels Severe acute respiratory syndrome coronavirus 2 Single-nucleotide polymorphism |
| title | Association of polymorphisms in long pentraxin 3 and its plasma levels with COVID-19 severity |
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