Syracuse

In vivo response of some immune and endocrine variables to LPS in Eurasian perch (Perca fluviatilis, L.) and modulation of this response by two corticosteroids, cortisol and 11-deoxycorticosterone

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Mathieu, Cédric | Milla, Sylvain | Mandiki, S. N. M. | Douxfils, Jessica | Kestemont, Patrick

Edité par CCSD ; Elsevier -

International audience. In fish, the endocrine system, especially corticosteroids pathway, strongly interacts with immune system. On the other hand, in vivo co-stimulation of both systems is not well documented. To better understand this interaction, we derided to evaluate the in vivo effects of both stimulation of the immune system and co-stimulation of both systems in Eurasian perch juveniles. Fish were injected either with 10 mg kg(-1) LPS, or with a combination of LPS and 0.8 mg kg(-1) cortisol or LPS and 0.08 mg kg(-1) 11-deoxycorticosterone (DOC) and sampled 1,3 or 7 days after injection. LPS affected the immune system by increasing plasma lysozyme activity and blood neutrophils populations. During the same time-course, LPS decreased the proportion of a mixture of lymphocytes and thrombocytes in blood and TNF-alpha expression in spleen. Cortisol modulated the LPS-mediated response in TNF-alpha mRNA expression levels in spleen. Contrary to LPS alone, the association of LPS with DOC modulated the abundance of complement component 3 (C3) mRNA in spleen. On the other hand, LPS altered the corticotropic axis by decreasing mRNA expression levels of all corticosteroid receptors and of 11 beta-HSD-2 in spleen. Both corticosteroids injected were not able to balance these LPS-induced suppressive effects on corticosteroid receptors and 11 beta-HSD-2 expression levels in spleen. Contrary to LPS alone, the association of LPS with DOC modulated GR-1b expression in gills. These results indicated that LPS is a strong modulator of the corticosteroid receptors expression in spleen. Furthermore, we report for the first time a LPS-induced decrease of the mineralocorticoid receptor expression. Finally, corticosteroids were able to modulate the LPS-mediated response at the transcriptional level.

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