期刊
COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY D-GENOMICS & PROTEOMICS
卷 7, 期 2, 页码 100-109出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cbd.2011.12.002
关键词
Inflammation; Lepeophtheirus salmonis; Salmonids; Immunomodulation; Innate immunity
资金
- Natural Sciences and Engineering Research Council (NSERC) of Canada [STPGP 372605-08]
- Fisheries and Oceans Canada
- Marine Harvest Canada (MHC)
Susceptibility among salmonids to the ectoparasite Lepeophtheirus salmonis is related to inflammatory reactions at the site of parasite attachment Salmon from two susceptible (Salmo salar, Oncorhynchus keta) and one resistant (Oncorhynchus gorbuscha) species were exposed to adult L salmonis. After 24 and 48 h. skin samples directly below the attachment site and at non-attachment sites were assessed for transcriptomic profiles of select innate defense genes. Abrasion of the skin permitted comparisons between abrasion-associated injury and louse-associated injury. Infection responses were consistently higher than those caused by abrasion. Temporal patterns of expression were evident in all species for the transcription factor CCAAT/enhancer-binding protein beta (C/EBP-beta), the cytokine interleukin-6 (IL-6) and the enzyme prostaglandin D synthase (PGDS) at attachment sites. O. gorbuscha was the highest responder in a number of genes while there was an absence of C-reactive protein (CRP) gene expression in S. solar and O. keta, indicating an altered acute-phase response. Moreover, O. keta displayed distinct interleukin-8 (IL-8) and serum amyloid P (SAP) responses. Impaired genetic expression or over-expression in these pathways may be evidence for species-specific pathways of susceptibility to the parasite. At L salmonis attachment sites, reduced expression compared to non-attachment sites was observed for C/EBP-beta (S. solar), CRP (S. salar), SAP (S. salar, O. gorbuscha, O. keta), PGDS (S. solar, O. gorbuscha, O. keta), and major histocompatibility class II (MH class II, S. salar), suggesting local immunodepression. Crown Copyright (C) 2011 Published by Elsevier Inc. All rights reserved.
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