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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| Published in | European journal of neurology Vol. 31; no. 2; pp. e16123 - n/a |
|---|---|
| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
John Wiley & Sons, Inc
01.02.2024
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| Subjects | |
| Online Access | Get full text |
| ISSN | 1351-5101 1468-1331 1468-1331 |
| DOI | 10.1111/ene.16123 |
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| 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. |
|---|---|
| AbstractList | 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. 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. 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. 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). 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. 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. 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.OBJECTIVESPrevious 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.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).METHODSTwo-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).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.RESULTSInverse 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.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.CONCLUSIONSThis 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. |
| Author | Liu, Zhaoxing Chen, Junqi Ding, Qian Zheng, Xiaoyan Huang, Yong Cai, Xiaowen Huang, Yumeng Huang, Shengtao Liu, Huacong Lai, Zhenyi Yin, Lianjun |
| Author_xml | – sequence: 1 givenname: Huacong orcidid: 0000-0002-2673-1827 surname: Liu fullname: Liu, Huacong organization: Southern Medical University – sequence: 2 givenname: Zhaoxing surname: Liu fullname: Liu, Zhaoxing organization: Southern Medical University – sequence: 3 givenname: Yumeng surname: Huang fullname: Huang, Yumeng organization: Southern Medical University – sequence: 4 givenname: Qian surname: Ding fullname: Ding, Qian organization: Southern Medical University – sequence: 5 givenname: Zhenyi surname: Lai fullname: Lai, Zhenyi organization: Southern Medical University – sequence: 6 givenname: Xiaowen surname: Cai fullname: Cai, Xiaowen organization: Southern Medical University – sequence: 7 givenname: Shengtao surname: Huang fullname: Huang, Shengtao organization: Southern Medical University – sequence: 8 givenname: Lianjun surname: Yin fullname: Yin, Lianjun organization: Third Affiliated Hospital of Southern Medical University – sequence: 9 givenname: Xiaoyan surname: Zheng fullname: Zheng, Xiaoyan email: zxy18825147762@smu.edu.cn organization: Southern Medical University – sequence: 10 givenname: Yong surname: Huang fullname: Huang, Yong email: nanfanglihuang@163.com organization: Southern Medical University – sequence: 11 givenname: Junqi surname: Chen fullname: Chen, Junqi email: meixibao@126.com organization: Southern Medical University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/37961927$$D View this record in MEDLINE/PubMed |
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| Keywords | functional outcomes GWAS Mendelian randomization inflammatory cytokines ischemic stroke |
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| Notes | Huacong Liu, Zhaoxing Liu, and Yumeng Huang contributed equally to this work and share first authorship. Xiaoyan Zheng, Yong Huang, and Junqi Chen contributed equally to this work and share last authorship. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
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Previous observational studies have indicated correlations between various inflammatory cytokines and functional outcomes following ischemic stroke... Previous observational studies have indicated correlations between various inflammatory cytokines and functional outcomes following ischemic stroke (IS);... Objectives Previous observational studies have indicated correlations between various inflammatory cytokines and functional outcomes following ischemic stroke... |
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| SubjectTerms | Cell activation Cytokines Eotaxin functional outcomes Genetic diversity Genomes GWAS Inflammation inflammatory cytokines Interleukin 18 Ischemia ischemic stroke Leukocytes (eosinophilic) Mendelian randomization Observational studies Randomization RANTES Stroke Variance analysis |
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| Title | Exploring causal association between circulating inflammatory cytokines and functional outcomes following ischemic stroke: A bidirectional Mendelian randomization study |
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