Transcriptional regulation of IL-17A and other inflammatory markers during the development of soybean meal-induced enteropathy in the distal intestine of Atlantic salmon (Salmo salar L.).
Progression of soybean meal (SBM)-induced enteropathy in Atlantic salmon (Salmo salar L.) distal intestine (DI) was studied to investigate pathophysiological mechanisms and immune responses. Seawater-adapted salmon were fed an extracted SBM-containing diet (200 g kg(-1)) from day 1-21 and compared with fish fed a fishmeal-based diet (day 0). Histological evaluation of the DI revealed signs of inflammation from day 5, which progressively increased in severity and affected more fish with increasing SBM exposure time. The expression profiles of 16 genes were analyzed by quantitative PCR. The pro-inflammatory cytokines interleukin 17A (IL-17A), IL-1β, interferon α (IFNα) and IFNγ, as well as IL-17A receptor, T-cell receptor γ (TCRγ), cluster of differentiation 4α (CD4α), CD8β, transforming growth factor β (TGFβ), trypsin, protease-activated receptor 2 (PAR2) and myeloid differentiation primary response gene 88 (MyD88) were significantly up-regulated during early and/or late inflammation stages, whereas interferon-γ-inducible lysosomal thiol reductase (GILT) was downregulated. Up-regulation of TCRγ from day seven suggests proliferation of intraepithelial γδ T cells. IL-17A, up-regulated by 218-fold during early inflammation, indicates involvement of T helper 17 cells in the pathogenesis of the SBM-induced inflammatory response.
Aquaculture Protein Centre (a Centre of Excellence), Department of Basic Sciences and Aquatic Medicine, Norwegian School of Veterinary Science, P.O. Box 8146 Dep., 0033 Oslo, Norway. Inderjit.mercy@gmail.com
Inderjit S
IS
Marjara
Elvis M
EM
Chikwati
Elin C
EC
Valen
Ashild
A
Krogdahl
Anne Marie
AM
Bakke
D000821:Animal Feed / Q000009:adverse effects; D000818:Animals; D016207:Cytokines / Q000235:genetics; D015536:Down-Regulation; D004751:Enteritis / Q000209:etiology / Q000235:genetics*; D005393:Fish Diseases / Q000209:etiology / Q000235:genetics*; D029941:Fish Proteins / Q000235:genetics*; D020869:Gene Expression Profiling; D018836:Inflammation Mediators / Q000378:metabolism*; D020381:Interleukin-17 / Q000235:genetics*; D053594:Myeloid Differentiation Factor 88 / Q000235:genetics; D050862:Oxidoreductases Acting on Sulfur Group Donors / Q000235:genetics; D044464:Receptor, PAR-2; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000235:genetics; D053722:Receptors, Interleukin-17 / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D020317:Salmo salar / Q000235:genetics*; D013025:Glycine max / Q000009:adverse effects; D013997:Time Factors; D014158:Transcription, Genetic; D015854:Up-Regulation
D016207:Cytokines; D029941:Fish Proteins; D018836:Inflammation Mediators; D020381:Interleukin-17; D053594:Myeloid Differentiation Factor 88; D044464:Receptor, PAR-2; D016692:Receptors, Antigen, T-Cell, gamma-delta; D053722:Receptors, Interleukin-17; D050862:Oxidoreductases Acting on Sulfur Group Donors