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Cortisol modulates the induction of inflammatory gene expression in a rainbow trout macrophage cell line

Rosario Castro1, Jun Zou, Christopher J Secombes

  • 1Scottish Fish Immunology Research Centre, Institute of Biological and Environmental Sciences, University of Aberdeen, Aberdeen, AB24 2TZ Scotland, UK. mrcastrosequ@jouy.inra.fr

Fish & Shellfish Immunology
|October 23, 2010
PubMed

Insights

Cortisol, a key hormone, generally suppresses inflammatory gene expression in rainbow trout macrophages. However, it synergistically enhances the expression of anti-inflammatory IL-10, suggesting a role in resolving inflammation.

Area of Science:

  • Immunology
  • Endocrinology
  • Aquatic Animal Health

Background:

  • Glucocorticoid effects on immune cells are diverse and cell-specific.
  • Limited understanding of hormone-cytokine interactions in fish macrophages.
  • Investigating cortisol's role in modulating inflammatory responses in fish.

Purpose of the Study:

  • To analyze gene expression patterns in rainbow trout macrophages (RTS-11) exposed to cortisol.
  • To assess cortisol's interaction with pro-inflammatory cytokines, type I IFN, and PAMPs.
  • To determine cortisol's effect on key inflammatory and anti-inflammatory genes.

Main Methods:

  • Quantitative PCR analysis of RTS-11 macrophage cell line.
  • Exposure to cortisol alone and in combination with recombinant trout IL-1β, IFN-γ, LPS, or poly I:C.
  • Gene expression analysis at 3 and 6 hours post-incubation.

Main Results:

  • Cortisol alone decreased IL-6 and IL-8 expression after 3-6 hours.
  • Co-stimulation with cortisol generally suppressed inflammatory gene upregulation (IL-8, IL-6, γIP, Cox-2).
  • Cortisol synergistically increased anti-inflammatory IL-10 expression with pro-inflammatory agents.

Conclusions:

  • Cortisol exerts a generally immunosuppressive effect on inflammatory gene expression in fish macrophages.
  • Cortisol promotes the resolution of inflammation by upregulating anti-inflammatory IL-10.
  • Demonstrates cell type-specific cross-talk between cortisol and cytokines in fish immune responses.

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