Title of article :
Modulation of cellular innate immunity by Lepeophtheirus salmonis secretory products
Author/Authors :
Lewis، نويسنده , , D.L. and Barker، نويسنده , , D.E. and McKinley، نويسنده , , R.S.، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2014
Pages :
9
From page :
175
To page :
183
Abstract :
Lepeophtheirus salmonis produces pharmacologically active substances that have been shown to modify genetic expression of inflammatory mediators in SHK-1 cells and head kidney macrophages of salmon. Differences in genetic expression among genera of Oncorhynchus and Salmo reflect different susceptibilities to L. salmonis. This study was conducted to determine if the presence of L. salmonis secretory products (SEPs)11  secretory products isolated from Lepeophtheirus salmonis. s the cellular innate immune response (specifically macrophage function) among several salmonids. Phagocytic assays were performed using SHK-1 cells and macrophages isolated from pink (Oncorhynchus gorbuscha), chum (Oncorhynchus keta) and Atlantic (Salmo salar) salmon following incubation with SEPs and Aeromonas salmonicida. Respiratory burst assays were analyzed using pink, chum and Atlantic salmon macrophages after exposure to SEPs. For SHK-1 cells, incubation with SEPS led to dose-dependent increases in phagocytosis. Following incubation with SEPs, chum salmon macrophages had the highest phagocytic index (55.1%) followed by Atlantic (26.4%) and pink (15.8%) salmon. In contrast, respiratory burst response was greatest in pink salmon and minimal in the other two species. Our results suggest that the cellular innate immune response of salmon is modified in the presence of L. salmonis secretions and differences observed among species provide insight into species-specific consequences of sea lice infection.
Keywords :
Lepeophtheirus salmonis , salmonids , macrophage , innate immunity , Immunomodulation
Journal title :
Fish and Shellfish Immunology
Serial Year :
2014
Journal title :
Fish and Shellfish Immunology
Record number :
2113103
Link To Document :
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