Surplus arginine reduced lipopolysaccharide induced transcription of proinflammatory genes in Atlantic salmon head kidney cells. Issue 86 (March 2019)

• Record Type: Journal Article
• Authors: Martins, Graciela P.; Espe, Marit; Zhang, Zhihao; Guimarães, Igo G.; Holen, Elisabeth
• Is Part Of: Fish & shellfish immunology. Issue 86(2019)
• Page Start: 1130
• Page End: 1138
• Publication Date: 2019-03
• Subjects: Cell culture -- Arginine -- Immunity -- Polyamine synthesis; Fishes -- Immunology -- Periodicals; Shellfish -- Immunology -- Periodicals; Poissons -- Immunologie -- Périodiques; Crustacés -- Immunologie -- Périodiques; 571.9617
• DOI: 10.1016/j.fsi.2018.12.043
• Languages: English
• ISSNs: 1050-4648

Abstract

Abstract: In aquaculture production, studies of salmon health and interaction between pathogens and nutrition are of high importance. This study aimed to compare genes and pathways involved in salmon head kidney cells and liver cells, isolated from the same fish, towards polyinosinic acid: polycytidylic acid (poly I:C) and lipopolysaccharide (LPS), with and without addition of surplus arginine. Selected transcriptional responses of genes involved in inflammation, polyamine synthesis, oxidation and apoptosis were elucidated. For the genes related to inflammation, viperin, Mx and Toll like receptor 3 ( TLR3), transcription were significantly upregulated by poly I:C in head kidney cells, while viperin was upregulated in liver cells. Surplus arginine did not affect poly I:C induced responses with the exception of reducing poly I:C induced Mx transcription in head kidney cells. Gene transcription of Interleukin 1β ( IL-1β ), Interleukin-8 ( IL-8 ) and cyclooxygenase 2 ( Cox2 ) were elevated during LPS treatment in all liver and head kidney cell cultures. In addition, LPS induced significantly, CD83 transcription in liver cells and TNF-α transcription in head kidney cells. Surplus arginine significantly reduced IL-8, Cox2 and TNF-α transcription in head kidney cells. LPS upregulated arginase in head kidney cells while poly I:C upregulated S-adenosyl methionine decarboxylase ( SAMdc ) transcription in liver cells. This suggests that LPS and poly I:C modulates genes involved in polyamine synthesis. In addition, in head kidney cells, surplus arginine, when cultured together with LPS, increased the transcription of ornithine decarboxylase ( ODC ) the limiting enzyme of polyamine synthesis. The genes involved with oxidation and apoptosis were not affect by any of the treatments in liver cells, while LPS decreased caspase 3 transcription in head kidney cells. In liver cells, protein expression of catalase was reduced by surplus arginine alone and when challenged with poly I:C. Both liver cells and head kidney cells isolated from the same individual fish responded to LPS and poly I:C, depending on the gene analyzed. Additionally, arginine could modulate transcription of pro-inflammatory genes induced by LPS in salmon immune cells, thus affecting salmon immunity. Highlights: Liver cells and head kidney cells isolated from the same fish responded to LPS and poly I:C. Surplus arginine reduced LPS induced transcription of IL-8, Cox2 and TNF-α in head kidney cells of salmon. LPS and poly I:C interferes with genes related to the polyamine synthesis pathway in the cells. Surplus arginine modulated expression of catalase enzyme in liver cell samples.