title: Racial differences in T-lymphocyte response to glucocorticoids.
abstract: BACKGROUND
  Asthma morbidity and mortality is increased in blacks.
  
  
  OBJECTIVE
  The primary objective of this cross-sectional study was to determine if blacks, asthmatic or nonasthmatic, displayed diminished T-lymphocyte response to glucocorticoids in vitro compared to their white counterparts. If differences were noted, this would suggest a racial predisposition to decreased glucocorticoid responsiveness among blacks.
  
  
  METHODS
  Asthmatic (n = 395, 27% blacks) and control (n = 202, 52% blacks) subjects recruited from National Jewish Medical and Research Center and from the surrounding community participated in the study. In vitro glucocorticoid responsiveness was determined by assessing the log-transformed concentration of dexamethasone required to suppress phytohemagglutinin-induced T-lymphocyte proliferation by 50% (log(10) IC(50)). Asthma medication history, atopic status, and spirometric lung function measures corrected for race were collected.
  
  
  RESULTS
  Black and white asthmatic subjects had similar FEV(1) percentage of predicted values and inhaled and oral glucocorticoid requirements. Black asthmatic subjects displayed significantly diminished glucocorticoid responsiveness compared to white asthmatic subjects, as follows: median (first, third quartile) log(10) IC(50) values of 1.00 nmol (0.48, 1.83) vs 0.78 nmol (0.29, 1.45) [p = 0.028]. Similar results were found between black and white control subjects, as follows: median, 1.26 nmol (0.70, 2.14) vs 0.95 nmol (0.55, 1.48) [p = 0.01]. Age, race, and basal T-lymphocyte activity were significantly positively correlated to the log(10) IC(50) values.
  
  
  CONCLUSIONS
  Our observation that black asthmatic subjects and non-asthmatic control subjects require greater concentrations of glucocorticoid in vitro to suppress T-lymphocyte activation suggests that blacks have a racial predisposition to diminished glucocorticoid responsiveness, which may contribute to their heightened asthma morbidity.
authors.affiliation: National Jewish Medical & Research Center, 1400 Jackson St J316, Denver, CO 80206, USA. covarr@njc.org
authors.forename: Monica J
authors.initials: MJ
authors.lastname: Federico
authors.forename: Ronina A
authors.initials: RA
authors.lastname: Covar
authors.forename: Eleanor E
authors.initials: EE
authors.lastname: Brown
authors.forename: Donald Y M
authors.initials: DY
authors.lastname: Leung
authors.forename: Joseph D
authors.initials: JD
authors.lastname: Spahn
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001249:Asthma / Q000235:genetics / Q000276:immunology*; D044383:Black People / Q000235:genetics*; D002648:Child; D002675:Child, Preschool; D003907:Dexamethasone / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D005260:Female; D005541:Forced Expiratory Volume / Q000235:genetics / Q000276:immunology; D015870:Gene Expression / Q000502:physiology; D020022:Genetic Predisposition to Disease / Q000235:genetics; D006801:Humans; D007108:Immune Tolerance / Q000187:drug effects / Q000235:genetics / Q000276:immunology; D066298:In Vitro Techniques; D020128:Inhibitory Concentration 50; D007378:Interleukins / Q000235:genetics; D008213:Lymphocyte Activation / Q000187:drug effects* / Q000235:genetics / Q000276:immunology; D008297:Male; D008875:Middle Aged; D012333:RNA, Messenger / Q000235:genetics; D012016:Reference Values; D012130:Respiratory Hypersensitivity / Q000235:genetics / Q000276:immunology; D013601:T-Lymphocytes / Q000187:drug effects* / Q000276:immunology; D044465:White People / Q000235:genetics*
chemical_list: D007378:Interleukins; D012333:RNA, Messenger; D003907:Dexamethasone