title: Amniotic fluid chemokines and autism spectrum disorders: an exploratory study utilizing a Danish Historic Birth Cohort.
abstract: BACKGROUND
  Elevated levels of chemokines have been reported in plasma and brain tissue of individuals with Autism Spectrum Disorders (ASD). The aim of this study was to examine chemokine levels in amniotic fluid (AF) samples of individuals diagnosed with ASD and their controls.
  
  
  METHODS
  A Danish Historic Birth Cohort (HBC) kept at Statens Serum Institute, Copenhagen was utilized. Using data from Danish nation-wide health registers, a case-control study design of 414 cases and 820 controls was adopted. Levels of MCP-1, MIP-1α and RANTES were analyzed using Luminex xMAP technology. Case-control differences were assessed as dichotomized at below the 10th percentile or above the 90th percentile cut-off points derived from the control biomarker distributions (logistic regression) or continuous measures (tobit regression).
  
  
  CONCLUSIONS
  AF volume for 331 cases and 698 controls was sufficient for Luminex analysis. Including all individuals in the cohort yielded no significant differences in chemokine levels in cases versus controls. Logistic regression analyses, performed on individuals diagnosed using ICD-10 only, showed increased risk for ASD with elevated MCP-1 (elevated 90th percentile adjusted OR: 2.32 [95% CI: 1.17-4.61]) compared to controls. An increased risk for infantile autism with elevated MCP-1 was also found (adjusted OR: 2.28 [95% CI: 1.16-4.48]). Elevated levels of MCP-1 may decipher an etiologic immunologic dysfunction or play rather an indirect role in the pathophysiology of ASD. Further studies to confirm its role and to identify the potential pathways through which MCP-1 may contribute to the development of ASD are necessary.
authors.affiliation: Department of Epidemiology, Aarhus University School of Public Health, Aarhus, Denmark. mab@soci.au.dk
authors.forename: Morsi W
authors.initials: MW
authors.lastname: Abdallah
authors.forename: Nanna
authors.initials: N
authors.lastname: Larsen
authors.forename: Jakob
authors.initials: J
authors.lastname: Grove
authors.forename: Bent
authors.initials: B
authors.lastname: Nørgaard-Pedersen
authors.forename: Poul
authors.initials: P
authors.lastname: Thorsen
authors.forename: Erik L
authors.initials: EL
authors.lastname: Mortensen
authors.forename: David M
authors.initials: DM
authors.lastname: Hougaard
mesh_terms: D000328:Adult; D000653:Amniotic Fluid / Q000378:metabolism*; D016022:Case-Control Studies; D018932:Chemokine CCL2 / Q000032:analysis / Q000378:metabolism; D054405:Chemokine CCL3 / Q000032:analysis / Q000378:metabolism; D018946:Chemokine CCL5 / Q000378:metabolism; D018925:Chemokines / Q000378:metabolism*; D002648:Child; D002659:Child Development Disorders, Pervasive / Q000453:epidemiology / Q000378:metabolism*; D015331:Cohort Studies; D000013:Congenital Abnormalities / Q000453:epidemiology; D003718:Denmark / Q000453:epidemiology; D005260:Female; D005865:Gestational Age; D006801:Humans; D038801:International Classification of Diseases; D016015:Logistic Models; D008423:Maternal Age; D001523:Mental Disorders / Q000453:epidemiology; D016017:Odds Ratio; D011247:Pregnancy
chemical_list: C111835:CCL2 protein, human; C515429:CCL3 protein, human; D018932:Chemokine CCL2; D054405:Chemokine CCL3; D018946:Chemokine CCL5; D018925:Chemokines