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-1β, tumor necrosis factor-α, serum amyloid A and inducible nitric oxide synthase. An NF-κB-inhibitor could replicate cortisol-induced apoptosis of activated peripheral blood leukocytes. In contrast, although this NF-κB-inhibitor induced apoptosis of neutrophilic granulocytes, cortisol prevented apoptosis of these cells, suggesting the latter process to be NF-κB-independent. Carp leukocytes, upon induction of apoptosis, exhibit a number of sequential metabolic alterations. First, the mitochondrial transmembrane potential (ΔΨm) 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 language | English (US) |
|---|---|
| Pages (from-to) | 233-245 |
| Number of pages | 13 |
| Journal | Developmental and Comparative Immunology |
| Volume | 27 |
| Issue number | 3 |
| DOIs | |
| State | Published - Mar 1 2003 |
| Externally published | Yes |
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Keywords
- Apoptosis
- Carp
- Cortisol
- Disease resistance
- Fish
- Glutathione depletion
- Kinetoplastida
- Stress
ASJC Scopus subject areas
- Developmental Biology
- Immunology
Cite this
Daily handling stress reduces resistance of carp to Trypanoplasma borreli : In vitro modulatory effects of cortisol on leukocyte function and apoptosis. / Saeij, Jeroen; Verburg-Van Kemenade, Lidy B M; Van Muiswinkel, Willem B.; Wiegertjes, Geert F.
In: Developmental and Comparative Immunology, Vol. 27, No. 3, 01.03.2003, p. 233-245.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Daily handling stress reduces resistance of carp to Trypanoplasma borreli
T2 - In vitro modulatory effects of cortisol on leukocyte function and apoptosis
AU - Saeij, Jeroen
AU - Verburg-Van Kemenade, Lidy B M
AU - Van Muiswinkel, Willem B.
AU - Wiegertjes, Geert F.
PY - 2003/3/1
Y1 - 2003/3/1
N2 - 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-1β, tumor necrosis factor-α, serum amyloid A and inducible nitric oxide synthase. An NF-κB-inhibitor could replicate cortisol-induced apoptosis of activated peripheral blood leukocytes. In contrast, although this NF-κB-inhibitor induced apoptosis of neutrophilic granulocytes, cortisol prevented apoptosis of these cells, suggesting the latter process to be NF-κB-independent. Carp leukocytes, upon induction of apoptosis, exhibit a number of sequential metabolic alterations. First, the mitochondrial transmembrane potential (ΔΨm) 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.
AB - 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-1β, tumor necrosis factor-α, serum amyloid A and inducible nitric oxide synthase. An NF-κB-inhibitor could replicate cortisol-induced apoptosis of activated peripheral blood leukocytes. In contrast, although this NF-κB-inhibitor induced apoptosis of neutrophilic granulocytes, cortisol prevented apoptosis of these cells, suggesting the latter process to be NF-κB-independent. Carp leukocytes, upon induction of apoptosis, exhibit a number of sequential metabolic alterations. First, the mitochondrial transmembrane potential (ΔΨm) 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.
KW - Apoptosis
KW - Carp
KW - Cortisol
KW - Disease resistance
KW - Fish
KW - Glutathione depletion
KW - Kinetoplastida
KW - Stress
UR - http://www.scopus.com/inward/record.url?scp=0037363749&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0037363749&partnerID=8YFLogxK
U2 - 10.1016/S0145-305X(02)00093-9
DO - 10.1016/S0145-305X(02)00093-9
M3 - Article
C2 - 12590974
AN - SCOPUS:0037363749
VL - 27
SP - 233
EP - 245
JO - Developmental and Comparative Immunology
JF - Developmental and Comparative Immunology
SN - 0145-305X
IS - 3
ER -