Abstract
Although immune endocrine interactions in teleost fish have been shown to involve adrenocorticotropin hormone (ACTH) and cortisol, the involvement of corticotropin-releasing hormone (CRH) has not been demonstrated. The present study investigates whether treatment with bacterial endotoxin (lipopolysaccharide, LPS) modulates brain CRH contents or in vitro CRH release in tilapia (Oreochromis mossambicus). 10 days LPS (Escherichia coli) exposure of juvenile tilapia (4.5 weeks post hatch) via the ambient water increased brain CRH and alpha-MSH content, whereas cortisol contents were not increased. This indicates that the elevation of brain CRH levels were not secondary to activation of HPI-axis. Adult tilapia were treated for 6 days with LPS (intraperitoneally) and were sampled before and after 24 h of confinement. Overall LPS pre-treatment modified the reaction of tilapia to the additional stressor of 24 h confinement, as interactions between LPS treatment and confinement were observed at the level of the hypothalamus (diencephalic CRH content), the pituitary (CRH and alpha-MSH content) and in plasma glucose levels. In vitro, LPS pre-treatment abolished CRH release from telencephalic tissues induced by norepinephrine, one of the CRH secretagogues released during stress in vivo. This effect might be a mechanism of action through which LPS in vivo abolished the up-regulation of telencephalic CRH induced by confinement stress. Our results provide evidence that the role of CRH in immune-endocrine interactions is a phylogenetically old mechanism, and we here demonstrate that LPS molecules are able to locally modulate CRH release in the central nervous system.
