Exploring causal association between circulating inflammatory cytokines and functional outcomes following ischemic stroke: A bidirectional Mendelian randomization study
Objectives Previous observational studies have indicated correlations between various inflammatory cytokines and functional outcomes following ischemic stroke (IS); however, the causality remains unclear. We aimed to further evaluate the causal association between 41 circulating inflammatory cytokin...
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| Veröffentlicht in: | European journal of neurology 2024-02, Vol.31 (2), p.e16123-n/a |
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| creator | Liu, Huacong Liu, Zhaoxing Huang, Yumeng Ding, Qian Lai, Zhenyi Cai, Xiaowen Huang, Shengtao Yin, Lianjun Zheng, Xiaoyan Huang, Yong Chen, Junqi |
| description | Objectives
Previous observational studies have indicated correlations between various inflammatory cytokines and functional outcomes following ischemic stroke (IS); however, the causality remains unclear. We aimed to further evaluate the causal association between 41 circulating inflammatory cytokines and functional outcomes following IS.
Methods
Two‐sample bidirectional Mendelian randomization (MR) analysis was used in this study. The genetic variation of 41 circulating inflammatory cytokines were derived from genome‐wide association study (GWAS) data of European ancestry (n = 8293). The corresponding genetic association of functional outcomes following IS were derived from European ancestry GWAS data (n = 6021).
Results
Inverse variance weighted (IVW) analysis showed that genetically predicted increased levels of regulation and activation in normal T‐cell expression and secretion factor (RANTES/CCL5) and eosinophilic chemotactic factor (EOTAXIN/CCL11) were positively correlated with the increased adverse functional outcomes (modified Rankin Scale [mRS≥3] following IS (OR: 1.40, 95% CI: 1.002–1.96, p = 0.049; OR: 1.33, 95% CI: 1.15–1.54, p = 0.0001). Interleukin 18 (IL‐18) level might be the downstream consequence of adverse functional outcomes following IS (β: −0.09, p = 0.039). Other inflammatory cytokines and functional outcomes following IS did not appear to be causally related.
Conclusions
This study suggests a causality between inflammation and adverse functional outcomes following IS. RANTES (CCL5) and EOTAXIN (CCL11) may be the upstream factors of adverse functional outcomes following IS, while IL‐18 may be the downstream effect of adverse functional outcomes following IS. Whether these cytokines can be used to predict or improve adverse functional outcomes after IS requires further researches. |
| doi_str_mv | 10.1111/ene.16123 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2889995620</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2889995620</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3883-4649160e874bda9acb434cc4c301cedbcf923cfe6566dd1d65a8cf796b3800583</originalsourceid><addsrcrecordid>eNp1kc1u1TAQRiMEoqWw4AWQJTawSGvHia_NrqouP1JpN7COnPEE3Dr2xY51SZ-Ix8Rt2i6Q8MbW6MzRjL-qes3oMSvnBD0eM8Ea_qQ6ZK2QNeOcPS1v3rG6Y5QdVC9SuqKUNpuGPq8O-EYJpprNYfVn-3vnQrT-BwGdk3ZEpxTA6tkGTwac94iegI2QXakVzPrR6WnSc4gLgWUO19ZjItobMmYPt33FEvIMYSr1MTgX9neNCX7iZIGkOYZr_EBOyWCNjfjQ8xW9QWe1J7HYwmRv1inSnM3ysno2apfw1f19VH3_uP129rk-v_z05ez0vAYuJa9b0SomKMpNOxitNAwtbwFa4JQBmgFG1XAYUXRCGMOM6LSEsXzHwCWlneRH1bvVu4vhV8Y091MZHJ3THkNOfSOlUqoTDS3o23_Qq5Bj2aRQijGhpKK8UO9XCmJIKeLY76KddFx6Rvvb-PoSX38XX2Hf3BvzMKF5JB_yKsDJCuytw-X_pn57sV2VfwEMOakq</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2911698903</pqid></control><display><type>article</type><title>Exploring causal association between circulating inflammatory cytokines and functional outcomes following ischemic stroke: A bidirectional Mendelian randomization study</title><source>MEDLINE</source><source>Wiley Online Library Open Access</source><source>Wiley Online Library Journals Frontfile Complete</source><source>PubMed Central</source><creator>Liu, Huacong ; Liu, Zhaoxing ; Huang, Yumeng ; Ding, Qian ; Lai, Zhenyi ; Cai, Xiaowen ; Huang, Shengtao ; Yin, Lianjun ; Zheng, Xiaoyan ; Huang, Yong ; Chen, Junqi</creator><creatorcontrib>Liu, Huacong ; Liu, Zhaoxing ; Huang, Yumeng ; Ding, Qian ; Lai, Zhenyi ; Cai, Xiaowen ; Huang, Shengtao ; Yin, Lianjun ; Zheng, Xiaoyan ; Huang, Yong ; Chen, Junqi</creatorcontrib><description>Objectives
Previous observational studies have indicated correlations between various inflammatory cytokines and functional outcomes following ischemic stroke (IS); however, the causality remains unclear. We aimed to further evaluate the causal association between 41 circulating inflammatory cytokines and functional outcomes following IS.
Methods
Two‐sample bidirectional Mendelian randomization (MR) analysis was used in this study. The genetic variation of 41 circulating inflammatory cytokines were derived from genome‐wide association study (GWAS) data of European ancestry (n = 8293). The corresponding genetic association of functional outcomes following IS were derived from European ancestry GWAS data (n = 6021).
Results
Inverse variance weighted (IVW) analysis showed that genetically predicted increased levels of regulation and activation in normal T‐cell expression and secretion factor (RANTES/CCL5) and eosinophilic chemotactic factor (EOTAXIN/CCL11) were positively correlated with the increased adverse functional outcomes (modified Rankin Scale [mRS≥3] following IS (OR: 1.40, 95% CI: 1.002–1.96, p = 0.049; OR: 1.33, 95% CI: 1.15–1.54, p = 0.0001). Interleukin 18 (IL‐18) level might be the downstream consequence of adverse functional outcomes following IS (β: −0.09, p = 0.039). Other inflammatory cytokines and functional outcomes following IS did not appear to be causally related.
Conclusions
This study suggests a causality between inflammation and adverse functional outcomes following IS. RANTES (CCL5) and EOTAXIN (CCL11) may be the upstream factors of adverse functional outcomes following IS, while IL‐18 may be the downstream effect of adverse functional outcomes following IS. Whether these cytokines can be used to predict or improve adverse functional outcomes after IS requires further researches.</description><identifier>ISSN: 1351-5101</identifier><identifier>ISSN: 1468-1331</identifier><identifier>EISSN: 1468-1331</identifier><identifier>DOI: 10.1111/ene.16123</identifier><identifier>PMID: 37961927</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Cell activation ; Cytokines ; Eotaxin ; functional outcomes ; Genetic diversity ; Genome-Wide Association Study ; Genomes ; GWAS ; Humans ; Inflammation ; inflammatory cytokines ; Interleukin 18 ; Ischemia ; Ischemic Stroke ; Leukocytes (eosinophilic) ; Mendelian randomization ; Mendelian Randomization Analysis ; Observational studies ; Randomization ; RANTES ; Stroke ; Variance analysis</subject><ispartof>European journal of neurology, 2024-02, Vol.31 (2), p.e16123-n/a</ispartof><rights>2023 The Authors. published by John Wiley & Sons Ltd on behalf of European Academy of Neurology.</rights><rights>2023 The Authors. European Journal of Neurology published by John Wiley & Sons Ltd on behalf of European Academy of Neurology.</rights><rights>2024. This work is published under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the "License"). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3883-4649160e874bda9acb434cc4c301cedbcf923cfe6566dd1d65a8cf796b3800583</citedby><cites>FETCH-LOGICAL-c3883-4649160e874bda9acb434cc4c301cedbcf923cfe6566dd1d65a8cf796b3800583</cites><orcidid>0000-0002-2673-1827</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fene.16123$$EPDF$$P50$$Gwiley$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fene.16123$$EHTML$$P50$$Gwiley$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,1411,11541,27901,27902,45550,45551,46027,46451</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37961927$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Huacong</creatorcontrib><creatorcontrib>Liu, Zhaoxing</creatorcontrib><creatorcontrib>Huang, Yumeng</creatorcontrib><creatorcontrib>Ding, Qian</creatorcontrib><creatorcontrib>Lai, Zhenyi</creatorcontrib><creatorcontrib>Cai, Xiaowen</creatorcontrib><creatorcontrib>Huang, Shengtao</creatorcontrib><creatorcontrib>Yin, Lianjun</creatorcontrib><creatorcontrib>Zheng, Xiaoyan</creatorcontrib><creatorcontrib>Huang, Yong</creatorcontrib><creatorcontrib>Chen, Junqi</creatorcontrib><title>Exploring causal association between circulating inflammatory cytokines and functional outcomes following ischemic stroke: A bidirectional Mendelian randomization study</title><title>European journal of neurology</title><addtitle>Eur J Neurol</addtitle><description>Objectives
Previous observational studies have indicated correlations between various inflammatory cytokines and functional outcomes following ischemic stroke (IS); however, the causality remains unclear. We aimed to further evaluate the causal association between 41 circulating inflammatory cytokines and functional outcomes following IS.
Methods
Two‐sample bidirectional Mendelian randomization (MR) analysis was used in this study. The genetic variation of 41 circulating inflammatory cytokines were derived from genome‐wide association study (GWAS) data of European ancestry (n = 8293). The corresponding genetic association of functional outcomes following IS were derived from European ancestry GWAS data (n = 6021).
Results
Inverse variance weighted (IVW) analysis showed that genetically predicted increased levels of regulation and activation in normal T‐cell expression and secretion factor (RANTES/CCL5) and eosinophilic chemotactic factor (EOTAXIN/CCL11) were positively correlated with the increased adverse functional outcomes (modified Rankin Scale [mRS≥3] following IS (OR: 1.40, 95% CI: 1.002–1.96, p = 0.049; OR: 1.33, 95% CI: 1.15–1.54, p = 0.0001). Interleukin 18 (IL‐18) level might be the downstream consequence of adverse functional outcomes following IS (β: −0.09, p = 0.039). Other inflammatory cytokines and functional outcomes following IS did not appear to be causally related.
Conclusions
This study suggests a causality between inflammation and adverse functional outcomes following IS. RANTES (CCL5) and EOTAXIN (CCL11) may be the upstream factors of adverse functional outcomes following IS, while IL‐18 may be the downstream effect of adverse functional outcomes following IS. Whether these cytokines can be used to predict or improve adverse functional outcomes after IS requires further researches.</description><subject>Cell activation</subject><subject>Cytokines</subject><subject>Eotaxin</subject><subject>functional outcomes</subject><subject>Genetic diversity</subject><subject>Genome-Wide Association Study</subject><subject>Genomes</subject><subject>GWAS</subject><subject>Humans</subject><subject>Inflammation</subject><subject>inflammatory cytokines</subject><subject>Interleukin 18</subject><subject>Ischemia</subject><subject>Ischemic Stroke</subject><subject>Leukocytes (eosinophilic)</subject><subject>Mendelian randomization</subject><subject>Mendelian Randomization Analysis</subject><subject>Observational studies</subject><subject>Randomization</subject><subject>RANTES</subject><subject>Stroke</subject><subject>Variance analysis</subject><issn>1351-5101</issn><issn>1468-1331</issn><issn>1468-1331</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kc1u1TAQRiMEoqWw4AWQJTawSGvHia_NrqouP1JpN7COnPEE3Dr2xY51SZ-Ix8Rt2i6Q8MbW6MzRjL-qes3oMSvnBD0eM8Ea_qQ6ZK2QNeOcPS1v3rG6Y5QdVC9SuqKUNpuGPq8O-EYJpprNYfVn-3vnQrT-BwGdk3ZEpxTA6tkGTwac94iegI2QXakVzPrR6WnSc4gLgWUO19ZjItobMmYPt33FEvIMYSr1MTgX9neNCX7iZIGkOYZr_EBOyWCNjfjQ8xW9QWe1J7HYwmRv1inSnM3ysno2apfw1f19VH3_uP129rk-v_z05ez0vAYuJa9b0SomKMpNOxitNAwtbwFa4JQBmgFG1XAYUXRCGMOM6LSEsXzHwCWlneRH1bvVu4vhV8Y091MZHJ3THkNOfSOlUqoTDS3o23_Qq5Bj2aRQijGhpKK8UO9XCmJIKeLY76KddFx6Rvvb-PoSX38XX2Hf3BvzMKF5JB_yKsDJCuytw-X_pn57sV2VfwEMOakq</recordid><startdate>202402</startdate><enddate>202402</enddate><creator>Liu, Huacong</creator><creator>Liu, Zhaoxing</creator><creator>Huang, Yumeng</creator><creator>Ding, Qian</creator><creator>Lai, Zhenyi</creator><creator>Cai, Xiaowen</creator><creator>Huang, Shengtao</creator><creator>Yin, Lianjun</creator><creator>Zheng, Xiaoyan</creator><creator>Huang, Yong</creator><creator>Chen, Junqi</creator><general>John Wiley & Sons, Inc</general><scope>24P</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-2673-1827</orcidid></search><sort><creationdate>202402</creationdate><title>Exploring causal association between circulating inflammatory cytokines and functional outcomes following ischemic stroke: A bidirectional Mendelian randomization study</title><author>Liu, Huacong ; Liu, Zhaoxing ; Huang, Yumeng ; Ding, Qian ; Lai, Zhenyi ; Cai, Xiaowen ; Huang, Shengtao ; Yin, Lianjun ; Zheng, Xiaoyan ; Huang, Yong ; Chen, Junqi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3883-4649160e874bda9acb434cc4c301cedbcf923cfe6566dd1d65a8cf796b3800583</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Cell activation</topic><topic>Cytokines</topic><topic>Eotaxin</topic><topic>functional outcomes</topic><topic>Genetic diversity</topic><topic>Genome-Wide Association Study</topic><topic>Genomes</topic><topic>GWAS</topic><topic>Humans</topic><topic>Inflammation</topic><topic>inflammatory cytokines</topic><topic>Interleukin 18</topic><topic>Ischemia</topic><topic>Ischemic Stroke</topic><topic>Leukocytes (eosinophilic)</topic><topic>Mendelian randomization</topic><topic>Mendelian Randomization Analysis</topic><topic>Observational studies</topic><topic>Randomization</topic><topic>RANTES</topic><topic>Stroke</topic><topic>Variance analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Huacong</creatorcontrib><creatorcontrib>Liu, Zhaoxing</creatorcontrib><creatorcontrib>Huang, Yumeng</creatorcontrib><creatorcontrib>Ding, Qian</creatorcontrib><creatorcontrib>Lai, Zhenyi</creatorcontrib><creatorcontrib>Cai, Xiaowen</creatorcontrib><creatorcontrib>Huang, Shengtao</creatorcontrib><creatorcontrib>Yin, Lianjun</creatorcontrib><creatorcontrib>Zheng, Xiaoyan</creatorcontrib><creatorcontrib>Huang, Yong</creatorcontrib><creatorcontrib>Chen, Junqi</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Huacong</au><au>Liu, Zhaoxing</au><au>Huang, Yumeng</au><au>Ding, Qian</au><au>Lai, Zhenyi</au><au>Cai, Xiaowen</au><au>Huang, Shengtao</au><au>Yin, Lianjun</au><au>Zheng, Xiaoyan</au><au>Huang, Yong</au><au>Chen, Junqi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Exploring causal association between circulating inflammatory cytokines and functional outcomes following ischemic stroke: A bidirectional Mendelian randomization study</atitle><jtitle>European journal of neurology</jtitle><addtitle>Eur J Neurol</addtitle><date>2024-02</date><risdate>2024</risdate><volume>31</volume><issue>2</issue><spage>e16123</spage><epage>n/a</epage><pages>e16123-n/a</pages><issn>1351-5101</issn><issn>1468-1331</issn><eissn>1468-1331</eissn><abstract>Objectives
Previous observational studies have indicated correlations between various inflammatory cytokines and functional outcomes following ischemic stroke (IS); however, the causality remains unclear. We aimed to further evaluate the causal association between 41 circulating inflammatory cytokines and functional outcomes following IS.
Methods
Two‐sample bidirectional Mendelian randomization (MR) analysis was used in this study. The genetic variation of 41 circulating inflammatory cytokines were derived from genome‐wide association study (GWAS) data of European ancestry (n = 8293). The corresponding genetic association of functional outcomes following IS were derived from European ancestry GWAS data (n = 6021).
Results
Inverse variance weighted (IVW) analysis showed that genetically predicted increased levels of regulation and activation in normal T‐cell expression and secretion factor (RANTES/CCL5) and eosinophilic chemotactic factor (EOTAXIN/CCL11) were positively correlated with the increased adverse functional outcomes (modified Rankin Scale [mRS≥3] following IS (OR: 1.40, 95% CI: 1.002–1.96, p = 0.049; OR: 1.33, 95% CI: 1.15–1.54, p = 0.0001). Interleukin 18 (IL‐18) level might be the downstream consequence of adverse functional outcomes following IS (β: −0.09, p = 0.039). Other inflammatory cytokines and functional outcomes following IS did not appear to be causally related.
Conclusions
This study suggests a causality between inflammation and adverse functional outcomes following IS. RANTES (CCL5) and EOTAXIN (CCL11) may be the upstream factors of adverse functional outcomes following IS, while IL‐18 may be the downstream effect of adverse functional outcomes following IS. Whether these cytokines can be used to predict or improve adverse functional outcomes after IS requires further researches.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>37961927</pmid><doi>10.1111/ene.16123</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-2673-1827</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Cell activation Cytokines Eotaxin functional outcomes Genetic diversity Genome-Wide Association Study Genomes GWAS Humans Inflammation inflammatory cytokines Interleukin 18 Ischemia Ischemic Stroke Leukocytes (eosinophilic) Mendelian randomization Mendelian Randomization Analysis Observational studies Randomization RANTES Stroke Variance analysis |
| title | Exploring causal association between circulating inflammatory cytokines and functional outcomes following ischemic stroke: A bidirectional Mendelian randomization study |
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