title: Increased T regulatory cells and decreased Th1 pro-inflammatory cytokines correlate with culture-positive infection in febrile neutropenia childhood oncology patients.
abstract: BACKGROUND
  Paediatric oncology patients with febrile neutropenia are usually hospitalised and treated with empirical broad-spectrum antibiotic therapy to counter the risk of infection. However, there is currently no method available to rapidly identify bacteremia in these patients. T-helper-type-1 (Th1) cytokines are required for effective immune response to many pathogenic organisms and T regulatory cells are known suppressors of Th1 cells. We hypothesized that characterization of reduced intracellular Th1 cytokines and increased T regulatory cells (Tregs) may prove useful in identifying infection in childhood oncology patients with febrile neutropenia.
  
  
  METHODS
  Intracellular Th 1 cytokines and Tregs were enumerated in peripheral blood from a group of childhood oncology patients with febrile neutropenia using multiparameter flow cytometry.
  
  
  RESULTS
  There was a significant increase in the percentage of CD25(+) CD127(-) CD8(-) CD3(+) Tregs and a significant decrease in Th1 intracellular cytokines IFNγ, IL-2 and TNFα in the blood of culture positive patients compared with culture negative patients.
  
  
  CONCLUSIONS
  Enumeration of Tregs and intracellular Th1 cytokines may provide a sensitive, specific test for determining infection in childhood oncology patients before blood culture results become available.
authors.affiliation: Haematology/Oncology Department, SA Pathology, Women's and Children's Hospital, North Adelaide 5006, Australia. greg.hodge@health.sa.gov.au
authors.forename: G
authors.initials: G
authors.lastname: Hodge
authors.forename: J
authors.initials: J
authors.lastname: Scott
authors.forename: M
authors.initials: M
authors.lastname: Osborn
authors.forename: L B
authors.initials: LB
authors.lastname: To
authors.forename: H
authors.initials: H
authors.lastname: Zola
authors.forename: S
authors.initials: S
authors.lastname: Hodge
authors.forename: T
authors.initials: T
authors.lastname: Revesz
mesh_terms: D016470:Bacteremia / Q000097:blood / Q000209:etiology; D017252:CD3 Complex / Q000378:metabolism; D016827:CD8 Antigens / Q000378:metabolism; D002478:Cells, Cultured; D002648:Child; D016207:Cytokines / Q000097:blood*; D005334:Fever / Q000097:blood / Q000209:etiology; D005434:Flow Cytometry; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D007371:Interferon-gamma / Q000097:blood; D007376:Interleukin-2 / Q000097:blood; D053645:Interleukin-2 Receptor alpha Subunit / Q000378:metabolism; D053699:Interleukin-7 Receptor alpha Subunit / Q000378:metabolism; D018655:Lymphocyte Count; D009369:Neoplasms / Q000097:blood* / Q000150:complications; D009503:Neutropenia / Q000097:blood* / Q000209:etiology; D050378:T-Lymphocytes, Regulatory / Q000378:metabolism*; D018417:Th1 Cells / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D017252:CD3 Complex; D016827:CD8 Antigens; D016207:Cytokines; D018836:Inflammation Mediators; D007376:Interleukin-2; D053645:Interleukin-2 Receptor alpha Subunit; D053699:Interleukin-7 Receptor alpha Subunit; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma