title: Augmented Th17-type immune responses in preterm neonates exposed to histologic chorioamnionitis.
abstract: BACKGROUND
  Histologic chorioamnionitis (HCA) is a placental inflammatory disorder that frequently precedes preterm delivery. HCA increases risk for long-standing inflammatory injury and may influence immune programming, particularly in preterm (PT) neonates. We hypothesized that HCA exposure is associated with an increased circulating frequency of proinflammatory, Th17-type responses.
  
  
  METHODS
  Placental cord blood was collected from HCA-exposed or control neonates (23-41 wk gestation). Frequencies of Th17 and T regulatory (Treg) cells and assessments of Th17-type features in CD4 and Treg cells were determined by flow cytometric analysis.
  
  
  RESULTS
  Cord blood samples from 31 PT and 17 term neonates were analyzed by flow cytometry. A diagnosis of HCA in extremely PT (EPT, GA ≤ 30 wk) gestations was associated with the highest cord blood frequencies of progenitor (pTh17, CD4+CD161+) and mature (mTh17, CD4+CD161+CCR6+) Th17 cells. Preterm neonates exposed to HCA also exhibited elevated cord blood frequencies of IL-17+Treg cells, as well as T cells with effector memory phenotype (TEM) that coexpressed Th17-type surface antigens.
  
  
  CONCLUSIONS
  Th17-type responses are amplified in preterm neonates exposed to HCA. We speculate that a Th17 bias may potentiate the inflammatory responses and related morbidity observed in preterm neonates whose immune systems have been "primed" by HCA exposure.
authors.affiliation: Department of Neonatology, Henry Ford Medical Group, Detroit, Michigan.
authors.forename: Daniel C
authors.initials: DC
authors.lastname: Rito
authors.affiliation: Department of Pediatrics, Saint Louis University, St. Louis, Missouri.
authors.forename: Luke T
authors.initials: LT
authors.lastname: Viehl
authors.affiliation: Department of Pediatrics, Saint Louis University, St. Louis, Missouri.|School of Public Health & Social Justice, Saint Louis University, St. Louis, Missouri.
authors.forename: Paula M
authors.initials: PM
authors.lastname: Buchanan
authors.affiliation: Department of Pediatrics, Saint Louis University, St. Louis, Missouri.
authors.forename: Seema
authors.initials: S
authors.lastname: Haridas
authors.affiliation: Department of Pediatrics, Saint Louis University, St. Louis, Missouri.|Department of Molecular Microbiology & Immunology, Saint Louis University, St. Louis, Missouri.
authors.forename: Joyce M
authors.initials: JM
authors.lastname: Koenig
mesh_terms: D000328:Adult; D015496:CD4-Positive T-Lymphocytes / Q000166:cytology; D016022:Case-Control Studies; D002821:Chorioamnionitis / Q000097:blood* / Q000276:immunology*; D005260:Female; D005312:Fetal Blood / Q000378:metabolism; D005434:Flow Cytometry; D006801:Humans; D007107:Immune System; D007231:Infant, Newborn; D007234:Infant, Premature; D007249:Inflammation; D020381:Interleukin-17 / Q000276:immunology; D010641:Phenotype; D010920:Placenta / Q000378:metabolism; D011247:Pregnancy; D011446:Prospective Studies; D050378:T-Lymphocytes, Regulatory / Q000166:cytology; D058504:Th17 Cells / Q000166:cytology*; D055815:Young Adult
chemical_list: C508717:IL17A protein, human; D020381:Interleukin-17