title: TH1/TH2 cytokine release pattern during in vivo cytomegalovirus disease in solid organ transplantation.
abstract: BACKGROUND
  Cytomegalovirus (CMV) disease is associated with an increased net immunosuppressive state in solid organ transplant recipients, leading to more bacterial and fungal infections. The release of pro- and anti-inflammatory cytokines could be one of the responsible factors.
  
  
  METHODS
  We prospectively included all patients undergoing solid organ transplantation between April and November 2004. During follow-up, plasma samples were collected in the immediate postsurgical period, at the first and second months, at the time of maximum antigenemia during CMV disease, and at 6 months posttransplantation. We determine the levels of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and IL-10. Log-transformed data were compared by a nonparametric Wilcoxon test for related variables.
  
  
  RESULTS
  During the study period, we monitored 146 recipients of solid organ transplantation: 77 kidneys, 8 kidney-pancreas, 46 liver, 11 heart, 2 liver-kidney, and 2 heart-kidney. No differences were observed between the TNF-alpha and IL-10 levels in the immediate postsurgical period or during CMV disease. TNF-alpha and IL-10 levels during CMV disease were higher than levels during the first month (mean TNF-alpha first month = 12.71 pg/mL vs CMV disease = 22.71 pg/mL, P = .028; mean IL-10 first month = 3.47 pg/mL vs CMV disease = 19.2 pg/mL, P = .018). Th1/Th2 ratio (measured as TNF-alpha/IL-10) was 1.75 in the immediate postsurgical period, 7.5 during the first month, 1.86 at the time of CMV disease, and 4.61 at the sixth month. The difference in Th1/Th2 ratio during CMV disease and in the first month was statistically significant (P = .043).
  
  
  CONCLUSIONS
  During CMV disease, we observed an increase in TNF-alpha and IL-10 release, which was similar to that during the postsurgical period. An imbalance toward an anti-inflammatory pattern was noted in these two periods. This could reflect a cooperative factor increasing the net state of immunosuppression during CMV disease.
authors: Infectious Diseases Service, Hospital Clínic, IDIBAPS, University of Barcelona, Barcelona, Spain. ccervera@clinic.ub.es
authors: C
authors: C
authors: Cervera
authors: X
authors: X
authors: Filella
authors: L
authors: L
authors: Linares
authors: M
authors: M
authors: Pineda
authors: C
authors: C
authors: Esteva
authors: A
authors: A
authors: Antón
authors: M A
authors: MA
authors: Marcos
authors: F
authors: F
authors: Cofán
authors: M
authors: M
authors: Navasa
authors: F
authors: F
authors: Pérez-Villa
authors: T
authors: T
authors: Pumarola
authors: A
authors: A
authors: Moreno
mesh_terms: D016207:Cytokines / Q000097:blood / Q000378:metabolism*; D003586:Cytomegalovirus Infections / Q000097:blood / Q000453:epidemiology / Q000276:immunology*; D005500:Follow-Up Studies; D006801:Humans; D016753:Interleukin-10 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D016377:Organ Transplantation / Q000706:statistics & numerical data*; D011446:Prospective Studies; D018417:Th1 Cells / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology*; D014181:Transplantation Immunology; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D016207:Cytokines; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10