DataSheet_1_Transcriptome Profiling of Atlantic Salmon (Salmo salar) Parr With Higher and Lower Pathogen Loads Following Piscirickettsia salmonis Infection.zip

Salmonid rickettsial septicemia (SRS), caused by Piscirickettsia salmonis, is one of the most devastating diseases of salmonids. However, the transcriptomic responses of Atlantic salmon (Salmon salar) in freshwater to an EM-90-like isolate have not been explored. Here, we infected Atlantic salmon parr with an EM-90-like isolate and conducted time-course qPCR analyses of pathogen load and four biomarkers (campb, hampa, il8a, tlr5a) of innate immunity on the head kidney samples. Transcript expression of three of these genes (except hampa), as well as pathogen level, peaked at 21 days post-injection (DPI). Multivariate analyses of infected individuals at 21 DPI revealed two infection phenotypes [lower (L-SRS) and higher (H-SRS) infection level]. Five fish from each group (Control, L-SRS, and H-SRS) were selected for transcriptome profiling using a 44K salmonid microarray platform. We identified 1,636 and 3,076 differentially expressed probes (DEPs) in the L-SRS and H-SRS groups compared with the control group, respectively (FDR = 1%). Gene ontology term enrichment analyses of SRS-responsive genes revealed the activation of a large number of innate (e.g. “phagocytosis”, “defense response to bacterium”, “inflammatory response”) and adaptive (e.g. “regulation of T cell activation”, “antigen processing and presentation of exogenous antigen”) immune processes, while a small number of general physiological processes (e.g. “apoptotic process”, development and metabolism relevant) was enriched. Transcriptome results were confirmed by qPCR analyses of 42 microarray-identified transcripts. Furthermore, the comparison of individuals with differing levels of infection (H-SRS vs. L-SRS) generated insights into the biological processes possibly involved in disease resistance or susceptibility. This study demonstrated a low mortality (~30%) EM-90-like infection model and broadened the current understanding of molecular pathways underlying P. salmonis-triggered responses of Atlantic salmon, identifying biomarkers that may assist to diagnose and combat this pathogen.

鲑立克次体败血症（Salmonid rickettsial septicemia, SRS）是由杀鲑立克次体（Piscirickettsia salmonis）引发的鲑科鱼类最具毁灭性的病害之一。然而，淡水环境中的大西洋鲑（Salmo salar，原文笔误为Salmon salar）对EM-90样分离株的转录组应答尚未被探索。本研究采用EM-90样分离株感染大西洋鲑幼鲑，并对头部肾脏样本开展了病原载量与4种先天免疫生物标志物（campb、hampa、il8a、tlr5a）的时序qPCR分析。结果显示，上述4种基因中除hampa外的3种基因的转录表达水平，以及病原载量，均在注射后21天（DPI）达到峰值。对21 DPI的感染个体进行多变量分析后，发现两类感染表型：低感染水平组（L-SRS）与高感染水平组（H-SRS）。本研究从对照组、L-SRS组与H-SRS组中各选取5尾个体，采用44K鲑科微阵列平台进行转录组分析。相较于对照组，L-SRS组与H-SRS组分别鉴定出1636个与3076个差异表达探针（differentially expressed probes, DEPs），错误发现率（FDR）为1%。对SRS应答基因开展基因本体（Gene Ontology, GO）富集分析发现，大量先天免疫过程（如"吞噬作用""细菌防御应答""炎症应答"）与适应性免疫过程（如"T细胞活化调控""外源性抗原的抗原加工与呈递"）被激活，同时少量通用生理过程（如"凋亡过程""发育与代谢相关过程"）也得到富集。通过对42个经微阵列筛选得到的转录本进行qPCR分析，验证了转录组结果的可靠性。此外，对不同感染水平个体（H-SRS与L-SRS）的比较分析，为阐明参与疾病抗性或易感性的生物学过程提供了新见解。本研究构建了死亡率约30%的EM-90样分离株感染模型，加深了当前对杀鲑立克次体诱导大西洋鲑应答的分子通路的认知，并鉴定出可用于该病原诊断与防控的生物标志物。