TH1/TH2 cytokine release pattern during in vivo cytomegalovirus disease in solid organ transplantation.

Published

Journal Article

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). CONCLUSION: 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.

Full Text

Cited Authors

  • Cervera, C; Filella, X; Linares, L; Pineda, M; Esteva, C; Antón, A; Marcos, MA; Cofán, F; Navasa, M; Pérez-Villa, F; Pumarola, T; Moreno, A

Published Date

  • September 2007

Published In

Volume / Issue

  • 39 / 7

Start / End Page

  • 2233 - 2235

PubMed ID

  • 17889148

Pubmed Central ID

  • 17889148

Electronic International Standard Serial Number (EISSN)

  • 1873-2623

International Standard Serial Number (ISSN)

  • 0041-1345

Digital Object Identifier (DOI)

  • 10.1016/j.transproceed.2007.07.048

Language

  • eng