Martinez Victor, Dettleff Phillip, Zamorano Pedro, Galarce Nicolás, Borie Consuelo, Naish Kerry
FAVET-INBIOGEN, Faculty of Veterinary Sciences, University of Chile, Avda. Santa Rosa, 11735, Santiago, Chile.
FAVET-INBIOGEN, Faculty of Veterinary Sciences, University of Chile, Avda. Santa Rosa, 11735, Santiago, Chile.
Fish Shellfish Immunol. 2023 May;136:108711. doi: 10.1016/j.fsi.2023.108711. Epub 2023 Mar 31.
The salmonid rickettsial syndrome (SRS) is a systemic bacterial infection caused by Piscirickettsia salmonis that generates significant economic losses in Atlantic salmon (Salmo salar) aquaculture. Despite this disease's relevance, the mechanisms involved in resistance against P. salmonis infection are not entirely understood. Thus, we aimed at studying the pathways explaining SRS resistance using different approaches. First, we determined the heritability using pedigree data from a challenge test. Secondly, a genome-wide association analysis was performed following a complete transcriptomic profile of fish from genetically susceptible and resistant families within the challenge infection with P. salmonis. We found differentially expressed transcripts related to immune response, pathogen recognition, and several new pathways related to extracellular matrix remodelling and intracellular invasion. The resistant background showed a constrained inflammatory response, mediated by the Arp2/3 complex actin cytoskeleton remodelling polymerization pathway, probably leading to bacterial clearance. A series of biomarkers of SRS resistance, such as the beta-enolase (ENO-β), Tubulin G1 (TUBG1), Plasmin (PLG) and ARP2/3 Complex Subunit 4 (ARPC4) genes showed consistent overexpression in resistant individuals, showing promise as biomarkers for SRS resistance. All these results together with the differential expression of several long non-coding RNAs show the complexity of the host-pathogen interaction of S. salar and P. salmonis. These results provide valuable information on new models describing host-pathogen interaction and its role in SRS resistance.
鲑鱼立克次氏体综合征（SRS）是一种由鲑鱼立克次氏体引起的全身性细菌感染，在大西洋鲑（Salmo salar）养殖中造成重大经济损失。尽管这种疾病具有重要意义，但抵抗鲑鱼立克次氏体感染的机制尚未完全明确。因此，我们旨在使用不同方法研究解释SRS抗性的途径。首先，我们利用来自攻毒试验的系谱数据确定了遗传力。其次，在对感染鲑鱼立克次氏体的遗传易感和抗性家系的鱼进行完整转录组分析后，进行了全基因组关联分析。我们发现了与免疫反应、病原体识别相关的差异表达转录本，以及与细胞外基质重塑和细胞内入侵相关的几个新途径。抗性背景表现出由Arp2/3复合肌动蛋白细胞骨架重塑聚合途径介导的受限炎症反应，这可能导致细菌清除。一系列SRS抗性生物标志物，如β-烯醇化酶（ENO-β）、微管蛋白G1（TUBG1）、纤溶酶（PLG）和ARP2/3复合亚基4（ARPC4）基因在抗性个体中表现出一致的过表达，有望作为SRS抗性的生物标志物。所有这些结果以及几种长链非编码RNA的差异表达显示了大西洋鲑和鲑鱼立克次氏体宿主-病原体相互作用的复杂性。这些结果为描述宿主-病原体相互作用及其在SRS抗性中的作用的新模型提供了有价值的信息。
