title: A genetic predisposition to produce low levels of IL-10 is related to depressive symptoms: a pilot study of patients with end stage renal disease.
abstract: OBJECTIVE
  Heightened levels of inflammation may be associated with an increased risk of depression, particularly among those with inflammatory medical conditions. Although elevated rates of both systemic inflammation and depression have been documented among patients with end stage renal disease (ESRD), the link between these factors has received little empirical evaluation. The goal of this pilot study was to investigate the association between cytokine gene polymorphisms (that are known to influence pro- and anti-inflammatory cytokine production) and depressive symptoms among patients with ESRD.
  
  
  METHODS
  Ninety-three patients with ESRD completed the Beck Depression Inventory-II and the disease-related symptom subscale of the Kidney Disease Quality of Life short form. Patients were genotyped for eight single nucleotide polymorphisms in genes coding for pro-inflammatory (TNF-α, IL-6, IFN-γ) and anti-inflammatory (IL-10, TGF-β1) cytokines.
  
  
  RESULTS
  Regression analyses indicated that patients with the A/A genotype for the IL-10 -1082 polymorphism (lower IL-10 producers) reported significantly greater depressive symptoms than G allele carriers (higher IL-10 producers; b = 0.22, P = 0.011), even after controlling for relevant covariates.
  
  
  CONCLUSIONS
  These findings provide some support for cytokine theories of depression in the medically ill, and specifically for the protective role of anti-inflammatory processes. Further research is needed to confirm these preliminary results and to explore the possibility of identifying subtypes of depressed patients based on inflammatory profiles, and those who may benefit from anti-inflammatory therapies.
authors.affiliation: Department of Psychology, University of British Columbia, Okanagan, Kelowna, BC, Canada. susan.holtzman@ubc.ca
authors.forename: Susan
authors.initials: S
authors.lastname: Holtzman
authors.forename: Susan E
authors.initials: SE
authors.lastname: Abbey
authors.forename: Christopher
authors.initials: C
authors.lastname: Chan
authors.forename: Joanne M
authors.initials: JM
authors.lastname: Bargman
authors.forename: Donna E
authors.initials: DE
authors.lastname: Stewart
mesh_terms: D000328:Adult; D000368:Aged; D000483:Alleles; D000704:Analysis of Variance; D016207:Cytokines / Q000235:genetics* / Q000378:metabolism; D003863:Depression / Q000453:epidemiology / Q000235:genetics* / Q000378:metabolism; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D007249:Inflammation / Q000235:genetics* / Q000378:metabolism; D016753:Interleukin-10 / Q000096:biosynthesis / Q000235:genetics*; D007676:Kidney Failure, Chronic / Q000453:epidemiology / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D010865:Pilot Projects; D020641:Polymorphism, Single Nucleotide; D011401:Promoter Regions, Genetic / Q000235:genetics
chemical_list: D016207:Cytokines; D016753:Interleukin-10