title: Genetic and environmental influences on pro-inflammatory monocytes in bipolar disorder: a twin study.
abstract: BACKGROUND
  A monocyte pro-inflammatory state has previously been reported in bipolar disorder (BD).
  
  
  OBJECTIVE
  To determine the contribution of genetic and environmental influences on the association between monocyte pro-inflammatory state and BD.
  
  
  METHODS
  A quantitative polymerase chain reaction case-control study of monocytes in bipolar twins. Determination of the influence of additive genetic, common, and unique environmental factors by structural equation modeling (ACE).
  
  
  METHODS
  Dutch academic research center.
  
  
  METHODS
  Eighteen monozygotic BD twin pairs, 23 dizygotic BD twin pairs, and 18 monozygotic and 16 dizygotic healthy twin pairs.
  
  
  METHODS
  Expression levels of monocytes in the previously reported coherent set of 19 genes (signature) reflecting the pro-inflammatory state.
  
  
  RESULTS
  The familial occurrence of the association between the monocyte pro-inflammatory gene-expression signature and BD found in the within-trait/cross-twin correlations (twin correlations) was due to shared environmental factors (ie, both monozygotic and dizygotic ratios in twin correlations approximated 1; ACE modeling data: 94% [95% confidence interval, 53%-99%] explained by common [shared] environmental factors). Although most individual signature genes followed this pattern, there was a small subcluster of genes in which genetic influences could dominate.
  
  
  CONCLUSIONS
  The association of the monocyte pro-inflammatory state with BD is primarily the result of a common shared environmental factor.
authors.affiliation: Department of Immunology, Erasmus Medical Center, 3000 DR Rotterdam, The Netherlands.
authors.forename: Roos C
authors.initials: RC
authors.lastname: Padmos
authors.forename: G Caroline M
authors.initials: GC
authors.lastname: Van Baal
authors.forename: Ronald
authors.initials: R
authors.lastname: Vonk
authors.forename: Annemarie J M
authors.initials: AJ
authors.lastname: Wijkhuijs
authors.forename: René S
authors.initials: RS
authors.lastname: Kahn
authors.forename: Willem A
authors.initials: WA
authors.lastname: Nolen
authors.forename: Hemmo A
authors.initials: HA
authors.lastname: Drexhage
mesh_terms: D000328:Adult; D000368:Aged; D001714:Bipolar Disorder / Q000097:blood / Q000453:epidemiology / Q000235:genetics*; D054703:Cyclic Nucleotide Phosphodiesterases, Type 4 / Q000235:genetics; D004200:Diseases in Twins / Q000097:blood / Q000453:epidemiology / Q000235:genetics; D004777:Environment; D005260:Female; D015870:Gene Expression / Q000235:genetics*; D020869:Gene Expression Profiling / Q000706:statistics & numerical data; D020022:Genetic Predisposition to Disease; D006801:Humans; D007249:Inflammation / Q000235:genetics; D008297:Male; D008875:Middle Aged; D008957:Models, Genetic; D009000:Monocytes / Q000378:metabolism / Q000502:physiology*; D009426:Netherlands / Q000453:epidemiology; D012307:Risk Factors; D014429:Twins, Dizygotic / Q000235:genetics; D014430:Twins, Monozygotic / Q000235:genetics
chemical_list: D054703:Cyclic Nucleotide Phosphodiesterases, Type 4; C517360:PDE4B protein, human