IL‐1β associations with posttraumatic epilepsy development: A genetics and biomarker cohort study

Summary Objective Posttraumatic epilepsy (PTE) is a significant complication following traumatic brain injury (TBI), yet the role of genetic variation in modulating PTE onset is unclear. We hypothesized that TBI‐induced inflammation likely contributes to seizure development. We assessed whether gene...

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Published inEpilepsia (Copenhagen) Vol. 55; no. 7; pp. 1109 - 1119
Main Authors Diamond, Matthew L., Ritter, Anne C., Failla, Michelle D., Boles, Jennifer A., Conley, Yvette P., Kochanek, Patrick M., Wagner, Amy K.
Format Journal Article
LanguageEnglish
Published United States 01.07.2014
Subjects
Adolescent
Adult
Aged
Biomarkers - blood
Biomarkers - cerebrospinal fluid
Cohort Studies
Epilepsy, Post-Traumatic - blood
Epilepsy, Post-Traumatic - cerebrospinal fluid
Epilepsy, Post-Traumatic - genetics
Female
Genetic Markers - genetics
Genetic variation
Genetic Variation - genetics
Humans
IL‐1β
Inflammation
Interleukin-1beta - blood
Interleukin-1beta - cerebrospinal fluid
Interleukin-1beta - genetics
Male
Middle Aged
Polymorphism, Single Nucleotide - genetics
Posttraumatic epilepsy
Traumatic brain injury
Young Adult
Inflammation
Posttraumatic epilepsy
Traumatic brain injury
IL-1β
Genetic variation
Online AccessGet full text

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Abstract Summary Objective Posttraumatic epilepsy (PTE) is a significant complication following traumatic brain injury (TBI), yet the role of genetic variation in modulating PTE onset is unclear. We hypothesized that TBI‐induced inflammation likely contributes to seizure development. We assessed whether genetic variation in the interleukin‐1beta (IL‐1β) gene, IL‐1β levels in cerebrospinal fluid (CSF) and serum, and CSF/serum IL‐1β ratios would predict PTE development post‐TBI. Methods We investigated PTE development in 256 Caucasian adults with moderate‐to‐severe TBI. IL‐1β tagging and functional single nucleotide polymorphisms (SNPs) were genotyped. Genetic variance and PTE development were assessed. Serum and CSF IL‐1β levels were collected from a subset of subjects (n = 59) during the first week postinjury and evaluated for their associations with IL‐1β gene variants, and also PTE. Temporally matched CSF/serum IL‐1β ratios were also generated to reflect the relative contribution of serum IL‐1β to CSF IL‐1β. Results Multivariate analysis showed that higher CSF/serum IL‐1β ratios were associated with increased risk for PTE over time (p = 0.008). Multivariate analysis for rs1143634 revealed an association between the CT genotype and increased PTE risk over time (p = 0.005). The CT genotype group also had lower serum IL‐1β levels (p = 0.014) and higher IL‐1β CSF/serum ratios (p = 0.093). Significance This is the first report implicating IL‐1β gene variability in PTE risk and linking (1) IL‐1β gene variation with serum IL‐1β levels observed after TBI and (2) IL‐1β ratios with PTE risk. Given these findings, we propose that genetic and IL‐1β ratio associations with PTE may be attributable to biologic variability with blood–brain barrier integrity during TBI recovery. These results provide a rationale for further studies (1) validating the impact of genetic variability on IL‐1β production after TBI, (2) assessing genetically mediated signaling mechanisms that contribute to IL‐1β CSF/serum associations with PTE, and (3) evaluating targeted IL‐1β therapies that reduce PTE. A PowerPoint slide summarizing this article is available for download in the Supporting Information section here.
AbstractList Summary Objective Posttraumatic epilepsy (PTE) is a significant complication following traumatic brain injury (TBI), yet the role of genetic variation in modulating PTE onset is unclear. We hypothesized that TBI‐induced inflammation likely contributes to seizure development. We assessed whether genetic variation in the interleukin‐1beta (IL‐1β) gene, IL‐1β levels in cerebrospinal fluid (CSF) and serum, and CSF/serum IL‐1β ratios would predict PTE development post‐TBI. Methods We investigated PTE development in 256 Caucasian adults with moderate‐to‐severe TBI. IL‐1β tagging and functional single nucleotide polymorphisms (SNPs) were genotyped. Genetic variance and PTE development were assessed. Serum and CSF IL‐1β levels were collected from a subset of subjects (n = 59) during the first week postinjury and evaluated for their associations with IL‐1β gene variants, and also PTE. Temporally matched CSF/serum IL‐1β ratios were also generated to reflect the relative contribution of serum IL‐1β to CSF IL‐1β. Results Multivariate analysis showed that higher CSF/serum IL‐1β ratios were associated with increased risk for PTE over time (p = 0.008). Multivariate analysis for rs1143634 revealed an association between the CT genotype and increased PTE risk over time (p = 0.005). The CT genotype group also had lower serum IL‐1β levels (p = 0.014) and higher IL‐1β CSF/serum ratios (p = 0.093). Significance This is the first report implicating IL‐1β gene variability in PTE risk and linking (1) IL‐1β gene variation with serum IL‐1β levels observed after TBI and (2) IL‐1β ratios with PTE risk. Given these findings, we propose that genetic and IL‐1β ratio associations with PTE may be attributable to biologic variability with blood–brain barrier integrity during TBI recovery. These results provide a rationale for further studies (1) validating the impact of genetic variability on IL‐1β production after TBI, (2) assessing genetically mediated signaling mechanisms that contribute to IL‐1β CSF/serum associations with PTE, and (3) evaluating targeted IL‐1β therapies that reduce PTE. A PowerPoint slide summarizing this article is available for download in the Supporting Information section here.
Posttraumatic epilepsy (PTE) is a significant complication following traumatic brain injury (TBI), yet the role of genetic variation in modulating PTE onset is unclear. We hypothesized that TBI-induced inflammation likely contributes to seizure development. We assessed whether genetic variation in the interleukin-1beta (IL-1β) gene, IL-1β levels in cerebrospinal fluid (CSF) and serum, and CSF/serum IL-1β ratios would predict PTE development post-TBI.OBJECTIVEPosttraumatic epilepsy (PTE) is a significant complication following traumatic brain injury (TBI), yet the role of genetic variation in modulating PTE onset is unclear. We hypothesized that TBI-induced inflammation likely contributes to seizure development. We assessed whether genetic variation in the interleukin-1beta (IL-1β) gene, IL-1β levels in cerebrospinal fluid (CSF) and serum, and CSF/serum IL-1β ratios would predict PTE development post-TBI.We investigated PTE development in 256 Caucasian adults with moderate-to-severe TBI. IL-1β tagging and functional single nucleotide polymorphisms (SNPs) were genotyped. Genetic variance and PTE development were assessed. Serum and CSF IL-1β levels were collected from a subset of subjects (n = 59) during the first week postinjury and evaluated for their associations with IL-1β gene variants, and also PTE. Temporally matched CSF/serum IL-1β ratios were also generated to reflect the relative contribution of serum IL-1β to CSF IL-1β.METHODSWe investigated PTE development in 256 Caucasian adults with moderate-to-severe TBI. IL-1β tagging and functional single nucleotide polymorphisms (SNPs) were genotyped. Genetic variance and PTE development were assessed. Serum and CSF IL-1β levels were collected from a subset of subjects (n = 59) during the first week postinjury and evaluated for their associations with IL-1β gene variants, and also PTE. Temporally matched CSF/serum IL-1β ratios were also generated to reflect the relative contribution of serum IL-1β to CSF IL-1β.Multivariate analysis showed that higher CSF/serum IL-1β ratios were associated with increased risk for PTE over time (p = 0.008). Multivariate analysis for rs1143634 revealed an association between the CT genotype and increased PTE risk over time (p = 0.005). The CT genotype group also had lower serum IL-1β levels (p = 0.014) and higher IL-1β CSF/serum ratios (p = 0.093).RESULTSMultivariate analysis showed that higher CSF/serum IL-1β ratios were associated with increased risk for PTE over time (p = 0.008). Multivariate analysis for rs1143634 revealed an association between the CT genotype and increased PTE risk over time (p = 0.005). The CT genotype group also had lower serum IL-1β levels (p = 0.014) and higher IL-1β CSF/serum ratios (p = 0.093).This is the first report implicating IL-1β gene variability in PTE risk and linking (1) IL-1β gene variation with serum IL-1β levels observed after TBI and (2) IL-1β ratios with PTE risk. Given these findings, we propose that genetic and IL-1β ratio associations with PTE may be attributable to biologic variability with blood-brain barrier integrity during TBI recovery. These results provide a rationale for further studies (1) validating the impact of genetic variability on IL-1β production after TBI, (2) assessing genetically mediated signaling mechanisms that contribute to IL-1β CSF/serum associations with PTE, and (3) evaluating targeted IL-1β therapies that reduce PTE.SIGNIFICANCEThis is the first report implicating IL-1β gene variability in PTE risk and linking (1) IL-1β gene variation with serum IL-1β levels observed after TBI and (2) IL-1β ratios with PTE risk. Given these findings, we propose that genetic and IL-1β ratio associations with PTE may be attributable to biologic variability with blood-brain barrier integrity during TBI recovery. These results provide a rationale for further studies (1) validating the impact of genetic variability on IL-1β production after TBI, (2) assessing genetically mediated signaling mechanisms that contribute to IL-1β CSF/serum associations with PTE, and (3) evaluating targeted IL-1β therapies that reduce PTE.
Posttraumatic epilepsy (PTE) is a significant complication following traumatic brain injury (TBI), yet the role of genetic variation in modulating PTE onset is unclear. We hypothesized that TBI-induced inflammation likely contributes to seizure development. We assessed whether genetic variation in the interleukin-1beta (IL-1β) gene, IL-1β levels in cerebrospinal fluid (CSF) and serum, and CSF/serum IL-1β ratios would predict PTE development post-TBI. We investigated PTE development in 256 Caucasian adults with moderate-to-severe TBI. IL-1β tagging and functional single nucleotide polymorphisms (SNPs) were genotyped. Genetic variance and PTE development were assessed. Serum and CSF IL-1β levels were collected from a subset of subjects (n = 59) during the first week postinjury and evaluated for their associations with IL-1β gene variants, and also PTE. Temporally matched CSF/serum IL-1β ratios were also generated to reflect the relative contribution of serum IL-1β to CSF IL-1β. Multivariate analysis showed that higher CSF/serum IL-1β ratios were associated with increased risk for PTE over time (p = 0.008). Multivariate analysis for rs1143634 revealed an association between the CT genotype and increased PTE risk over time (p = 0.005). The CT genotype group also had lower serum IL-1β levels (p = 0.014) and higher IL-1β CSF/serum ratios (p = 0.093). This is the first report implicating IL-1β gene variability in PTE risk and linking (1) IL-1β gene variation with serum IL-1β levels observed after TBI and (2) IL-1β ratios with PTE risk. Given these findings, we propose that genetic and IL-1β ratio associations with PTE may be attributable to biologic variability with blood-brain barrier integrity during TBI recovery. These results provide a rationale for further studies (1) validating the impact of genetic variability on IL-1β production after TBI, (2) assessing genetically mediated signaling mechanisms that contribute to IL-1β CSF/serum associations with PTE, and (3) evaluating targeted IL-1β therapies that reduce PTE.
Posttraumatic epilepsy (PTE) is a significant complication following traumatic brain injury (TBI), yet the role of genetic variation in modulating PTE onset is unclear. We hypothesized that TBI-induced inflammation likely contributes to seizure development. We assessed whether genetic variation in the interleukin-1beta (IL-1 beta ) gene, IL-1 beta levels in cerebrospinal fluid (CSF) and serum, and CSF/serum IL-1 beta ratios would predict PTE development post-TBI. We investigated PTE development in 256 Caucasian adults with moderate-to-severe TBI. IL-1 beta tagging and functional single nucleotide polymorphisms (SNPs) were genotyped. Genetic variance and PTE development were assessed. Serum and CSF IL-1 beta levels were collected from a subset of subjects (n = 59) during the first week postinjury and evaluated for their associations with IL-1 beta gene variants, and also PTE. Temporally matched CSF/serum IL-1 beta ratios were also generated to reflect the relative contribution of serum IL-1 beta to CSF IL-1 beta . Multivariate analysis showed that higher CSF/serum IL-1 beta ratios were associated with increased risk for PTE over time (p = 0.008). Multivariate analysis for rs1143634 revealed an association between the CT genotype and increased PTE risk over time (p = 0.005). The CT genotype group also had lower serum IL-1 beta levels (p = 0.014) and higher IL-1 beta CSF/serum ratios (p = 0.093). This is the first report implicating IL-1 beta gene variability in PTE risk and linking (1) IL-1 beta gene variation with serum IL-1 beta levels observed after TBI and (2) IL-1 beta ratios with PTE risk. Given these findings, we propose that genetic and IL-1 beta ratio associations with PTE may be attributable to biologic variability with blood-brain barrier integrity during TBI recovery. These results provide a rationale for further studies (1) validating the impact of genetic variability on IL-1 beta production after TBI, (2) assessing genetically mediated signaling mechanisms that contribute to IL-1 beta CSF/serum associations with PTE, and (3) evaluating targeted IL-1 beta therapies that reduce PTE. A PowerPoint slide summarizing this article is available for download in the Supporting Information section here.
Author Failla, Michelle D.
Boles, Jennifer A.
Ritter, Anne C.
Kochanek, Patrick M.
Wagner, Amy K.
Diamond, Matthew L.
Conley, Yvette P.
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  fullname: Ritter, Anne C.
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  givenname: Michelle D.
  surname: Failla
  fullname: Failla, Michelle D.
  organization: University of Pittsburgh
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  givenname: Jennifer A.
  surname: Boles
  fullname: Boles, Jennifer A.
  organization: University of Pittsburgh
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  fullname: Conley, Yvette P.
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  givenname: Patrick M.
  surname: Kochanek
  fullname: Kochanek, Patrick M.
  organization: University of Pittsburgh
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  givenname: Amy K.
  surname: Wagner
  fullname: Wagner, Amy K.
  organization: University of Pittsburgh
BackLink https://www.ncbi.nlm.nih.gov/pubmed/24754437$$D View this record in MEDLINE/PubMed
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Issue 7
Keywords Inflammation
Posttraumatic epilepsy
Traumatic brain injury
IL-1β
Genetic variation
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Wiley Periodicals, Inc. © 2014 International League Against Epilepsy.
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Snippet Summary Objective Posttraumatic epilepsy (PTE) is a significant complication following traumatic brain injury (TBI), yet the role of genetic variation in...
Posttraumatic epilepsy (PTE) is a significant complication following traumatic brain injury (TBI), yet the role of genetic variation in modulating PTE onset is...
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Publisher
StartPage 1109
SubjectTerms Adolescent
Adult
Aged
Biomarkers - blood
Biomarkers - cerebrospinal fluid
Cohort Studies
Epilepsy, Post-Traumatic - blood
Epilepsy, Post-Traumatic - cerebrospinal fluid
Epilepsy, Post-Traumatic - genetics
Female
Genetic Markers - genetics
Genetic variation
Genetic Variation - genetics
Humans
IL‐1β
Inflammation
Interleukin-1beta - blood
Interleukin-1beta - cerebrospinal fluid
Interleukin-1beta - genetics
Male
Middle Aged
Polymorphism, Single Nucleotide - genetics
Posttraumatic epilepsy
Traumatic brain injury
Young Adult
Title IL‐1β associations with posttraumatic epilepsy development: A genetics and biomarker cohort study
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fepi.12628
https://www.ncbi.nlm.nih.gov/pubmed/24754437
https://www.proquest.com/docview/1547544855
https://www.proquest.com/docview/1551639436
Volume 55
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