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Effects of Moritella viscosa antigens on pro-inflammatory gene expression in an Atlantic salmon ( Salmo salar Linnaeus) cell line (SHK-1)
Moritella viscosa is the causative agent of winter ulcer disease in salmonids reared in North-Atlantic countries. In this study the effects of selected M. viscosa antigens on cytotoxicity and pro-inflammatory gene expression in an Atlantic salmon ( Salmo salar Linnaeus) macrophage-like cell line (SH...
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Published in: | Fish & shellfish immunology 2009-06, Vol.26 (6), p.858-863 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Moritella viscosa is the causative agent of winter ulcer disease in salmonids reared in North-Atlantic countries. In this study the effects of selected
M. viscosa antigens on cytotoxicity and pro-inflammatory gene expression in an Atlantic salmon (
Salmo salar Linnaeus) macrophage-like cell line (SHK-1) were examined. SHK-1 cells were stimulated with live and heat-killed bacterial cells, extracellular products (ECP) and an extracellular vibriolysin, termed MvP1. Following incubation, cytotoxicity and expression levels of interleukin-1β (IL-1β) and interleukin-8 (IL-8) were examined at different time points. Both live
M. viscosa cells and ECP were cytotoxic, but neither heat-killed cells, nor the MvP1 peptidase caused cell death. Expression levels of both IL-1β and IL-8 increased significantly after stimulation with live cells, but heat-killed cells only caused increased IL-8 expression. ECP did not affect IL-1β expression, but did stimulate IL-8 expression. The isolated MvP1 peptidase stimulated both IL-1β and IL-8 expression at the highest concentration tested. This study reveals a difference in the induction of pro-inflammatory gene expression in salmon SHK-1 cells between live and heat-killed
M. viscosa cells, and also that an unknown secreted factor is the main stimulant of IL-β and IL-8 expression. |
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ISSN: | 1050-4648 1095-9947 |
DOI: | 10.1016/j.fsi.2009.03.015 |