AI Article Synopsis

  • The study investigates how cytokine profiles differ between pediatric and adult patients with Crohn disease (CD), revealing potential differences in disease mechanisms.
  • In both age groups, patients with CD had higher levels of TNF-α-producing T cells compared to healthy controls, indicating an immune response in CD.
  • Pediatric patients showed lower levels of IFN-γ, suggesting distinct immunological differences in how CD manifests in children versus adults.

Article Abstract

Background: Increasing evidence suggests that cytokine dysregulation in T-helper 1 and T-helper 2 (TH1/TH2) subsets contributes to the pathogenesis of Crohn disease (CD). The present pilot study examines the hypothesis that cytokine profiles differ between pediatric and adult patients with CD.

Methods: Production of TH1 cytokines interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α) and of TH2 cytokines interleukin-4 (IL-4) and IL-6 was analyzed in peripheral blood of patients with CD and healthy controls (n=20) using flow cytometry after in vitro stimulation.

Results: In both pediatric and adult subjects, frequencies of TNF-α CD4+ T cells were higher in patients with CD than in controls (P=0.009 and P=0.047, respectively). Percentages of cells expressing IL-4 were slightly increased (P=0.036), whereas those for IFN-γ were decreased (P=0.009) in pediatric patients with CD compared with controls. As expected, the overall production of TH1 cytokines was higher in adults compared with pediatric subjects. When memory CD4+CD45RO+ T cells were considered, lower IFN-γ expression was observed in pediatric subjects with CD compared with controls (P=0.009), matching the trend seen in the general CD4+ T cell population. The percentage of CD4+CD45RO+ T cells was increased in adult patients with CD compared with pediatric patients with CD (P=0.016).

Conclusions: The present study describes a peripheral blood TH1/TH2 cytokine imbalance in CD and suggests different immunological mechanisms in children and adults for disease pathogenesis.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3339044PMC
http://dx.doi.org/10.1097/MPG.0b013e3182455bb3DOI Listing

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