Daily handling stress reduces carp disease resistance: modulatory effects of cortisol on apoptosis and in vitro leukocyte functions

J.P.J. Saeij, B.M.L. Verburg-van Kemenade, W.B. van Muiswinkel, G.F. Wiegertjes

Research output: Contribution to journalArticleAcademicpeer-review

88 Citations (Scopus)

Abstract

Carp subjected to daily handling stress were much more susceptible to Trypanoplasma borreli infection than control fish. In a search for the cellular mechanisms involved, it was observed that cortisol suppressed T. borreli-induced expression of interleukin-1ß, tumor necrosis factor-a, serum amyloid A and inducible nitric oxide synthase. An NF-¿B-inhibitor could replicate cortisol-induced apoptosis of activated peripheral blood leukocytes. In contrast, although this NF-¿B-inhibitor induced apoptosis of neutrophilic granulocytes, cortisol prevented apoptosis of these cells, suggesting the latter process to be NF-¿B-independent. Carp leukocytes, upon induction of apoptosis, exhibit a number of sequential metabolic alterations. First, the mitochondrial transmembrane potential (¿¿m) is disrupted and glutathione levels are depleted, followed by exposure of phosphatidylserine on the outer cell membrane. In vitro, cortisol could inhibit NO production induced by low concentrations of lipopolysaccharide (LPS), but remarkably, enhanced NO production induced by high concentrations of LPS. However, no differences in NO production were observed in stressed versus non-stressed infected carp.
Original languageEnglish
Pages (from-to)233-245
Number of pages13
JournalDevelopmental and Comparative Immunology
Volume27
Issue number3
DOIs
Publication statusPublished - 2003

Keywords

  • factor-kappa-b
  • common carp
  • cyprinus-carpio
  • in-vitro
  • neutrophilic granulocytes
  • plasma-cortisol
  • nitric-oxide
  • fish
  • glutathione
  • overexpression

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