Daily handling stress reduces resistance of carp to Trypanoplasma borreli: in vitro modulatory effects of cortisol on leukocyte function and apoptosis.
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-1beta, tumor necrosis factor-alpha, serum amyloid A and inducible nitric oxide synthase. An NF-kappaB-inhibitor could replicate cortisol-induced apoptosis of activated peripheral blood leukocytes. In contrast, although this NF-kappaB-inhibitor induced apoptosis of neutrophilic granulocytes, cortisol prevented apoptosis of these cells, suggesting the latter process to be NF-kappaB-independent. Carp leukocytes, upon induction of apoptosis, exhibit a number of sequential metabolic alterations. First, the mitochondrial transmembrane potential (DeltaPsi(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.
Saeij
Jeroen P J
JP
Cell Biology and Immunology Group, Wageningen Institute of Animal Sciences, Wageningen University, P.O. Box 338, 6700 AH Wageningen, The Netherlands.
Verburg-van Kemenade
Lidy B M
LB
van Muiswinkel
Willem B
WB
Wiegertjes
Geert F
GF
D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D002347:Carps / Q000276:immunology* / Q000469:parasitology*; D020169:Caspases / Q000502:physiology; D016207:Cytokines / Q000235:genetics; D004198:Disease Susceptibility; D005978:Glutathione / Q000032:analysis; D016830:Kinetoplastida / Q000276:immunology*; D007962:Leukocytes / Q000187:drug effects* / Q000276:immunology; D008564:Membrane Potentials; D008928:Mitochondria / Q000502:physiology; D009569:Nitric Oxide / Q000096:biosynthesis; D013312:Stress, Physiological / Q000276:immunology*; D014158:Transcription, Genetic / Q000187:drug effects
D016207:Cytokines; D009569:Nitric Oxide; D020169:Caspases; D005978:Glutathione