Eslamloo Khalil, Kumar Surendra, Xue Xi, Parrish Kathleen S, Purcell Sara L, Fast Mark D, Rise Matthew L
Department of Ocean Sciences, Memorial University of Newfoundland, St. John's, NL, Canada.
Hoplite Laboratory, Department of Pathology and Microbiology, Atlantic Veterinary College, University of Prince Edward Island, Charlottetown, PEI, Canada.
Sci Rep. 2022 Mar 17;12(1):4622. doi: 10.1038/s41598-022-08341-7.
Moritella viscosa is a Gram-negative pathogen that causes large, chronic ulcers, known as winter-ulcer disease, in the skin of several fish species including Atlantic salmon. We used a bath challenge approach to profile the transcriptome responses of M. viscosa-infected Atlantic salmon skin at the lesion (Mv-At) and away from the lesion (Mv-Aw) sites. M. viscosa infection was confirmed through RNA-based qPCR assays. RNA-Seq identified 5212 and 2911 transcripts differentially expressed in the Mv-At compared to no-infection control and Mv-Aw groups, respectively. Also, there were 563 differentially expressed transcripts when comparing the Mv-Aw to control samples. Our results suggest that M. viscosa caused massive and strong, but largely infection site-focused, transcriptome dysregulations in Atlantic salmon skin, and its effects beyond the skin lesion site were comparably subtle. The M. viscosa-induced transcripts of Atlantic salmon were mainly involved in innate and adaptive immune response-related pathways, whereas the suppressed transcripts by this pathogen were largely connected to developmental and cellular processes. As validated by qPCR, M. viscosa dysregulated transcripts encoding receptors, signal transducers, transcription factors and immune effectors playing roles in TLR- and IFN-dependent pathways as well as immunoregulation, antigen presentation and T-cell development. This study broadened the current understanding of molecular pathways underlying M. viscosa-triggered responses of Atlantic salmon, and identified biomarkers that may assist to diagnose and combat this pathogen.
粘滑莫拉菌是一种革兰氏阴性病原体，可在包括大西洋鲑鱼在内的几种鱼类的皮肤中引发大面积的慢性溃疡，即所谓的冬季溃疡病。我们采用浸浴攻毒法，分析了感染粘滑莫拉菌的大西洋鲑鱼皮肤在损伤部位（Mv-At）和非损伤部位（Mv-Aw）的转录组反应。通过基于RNA的定量PCR分析确认了粘滑莫拉菌感染。RNA测序分别鉴定出与未感染对照组和Mv-Aw组相比，在Mv-At中有5212个和2911个转录本差异表达。此外，将Mv-Aw与对照样本进行比较时，有563个差异表达的转录本。我们的结果表明，粘滑莫拉菌在大西洋鲑鱼皮肤中引起了大规模且强烈的转录组失调，但主要集中在感染部位，其对皮肤损伤部位以外的影响相对较小。粘滑莫拉菌诱导的大西洋鲑鱼转录本主要参与先天和适应性免疫反应相关途径，而该病原体抑制的转录本主要与发育和细胞过程相关。经定量PCR验证，粘滑莫拉菌使编码在TLR和IFN依赖性途径以及免疫调节、抗原呈递和T细胞发育中起作用的受体、信号转导器、转录因子和免疫效应器的转录本失调。本研究拓宽了当前对粘滑莫拉菌引发大西洋鲑鱼反应的分子途径的理解，并鉴定出可能有助于诊断和对抗这种病原体的生物标志物。
