Immune gene expression profiling of Proliferative Kidney Disease in rainbow trout Oncorhynchus mykiss reveals a dominance of anti-inflammatory, antibody and T helper cell-like activities.

Immune gene expression profiling of Proliferative Kidney Disease in rainbow trout Oncorhynchus mykiss reveals a dominance of anti-inflammatory, antibody and T helper cell-like activities.
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DOI:
10.1186/1297-9716-44-55
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发表时间:
2013-07-16
影响因子:
4.4
通讯作者:
Holland JW
Holland JW
中科院分区:
农林科学2区
文献类型:
--
作者:
Gorgoglione B;Wang T;Secombes CJ;Holland JW

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黏液动物四类苔藓沙门氏菌是增生性肾脏疾病(PKD)的病原体,主要针对受感染的鱼的肾脏,在那里它引起慢性淋巴细胞免疫病理。虽然已知与先天免疫的某些细胞方面的抑制和突出的淋巴细胞增生有关,但我们对驱动PKD发病的潜在免疫机制的理解仍然存在相当大的知识差距。为了提供进一步的见解,在自然暴露于寄生虫后,在虹鳟鱼Oncorhynchus mykiss中检测了一组先天/炎症和适应性免疫分子的表达谱。与对照组相比,早期到晚期肾脏病理的鱼表现出炎症细胞因子白介素(IL)-6和IL-11的上调,尽管对巨噬细胞活性的指示基因仍然难以抑制。抗菌肽(AMPs)和抗炎标志物,包括cathelicidin (CATH)和IL-10在临床疾病期间明显上调。适应性免疫分子的上调,包括细胞标记物和抗体基因,反映了这种疾病的淋巴细胞优势,以及淋巴细胞亚群在PKD发病机制中的可能重要性。T辅助细胞(TH)样反应基因和转录因子的上调表明,苔藓沙门氏菌可能引发TH细胞亚群之间复杂的相互作用。这项研究首次在鱼-黏液动物相互作用的研究中表明,PKD的发病机制是由抗炎表型、深刻的B细胞/抗体反应和异常的TH细胞样活性决定的。更好地了解鱼类免疫细胞和分子在PKD发病机制中的功能作用,可能有助于未来制定针对该疾病的控制措施。
The myxozoan Tetracapsuloides bryosalmonae is the causative agent of Proliferative Kidney Disease (PKD) targeting primarily the kidney of infected fish where it causes a chronic lymphoid immunopathology. Although known to be associated with suppression of some cellular aspects of innate immunity and a prominent lymphocytic hyperplasia, there remains a considerable knowledge gap in our understanding of the underlying immune mechanisms driving PKD pathogenesis. To provide further insights, the expression profiles of a panel of innate / inflammatory and adaptive immune molecules were examined in rainbow trout Oncorhynchus mykiss following a natural exposure to the parasite. Relative to controls, fish with early to advanced stages of kidney pathology exhibited up-regulation of the inflammatory cytokines interleukin (IL)-6 and IL-11, although remaining refractory towards genes indicative of macrophage activity. Antimicrobial peptides (AMPs) and anti-inflammatory markers, including cathelicidin (CATH) and IL-10 were markedly up-regulated during clinical disease. Up-regulation of adaptive immune molecules, including cell markers and antibody genes reflect the lymphocytic dominance of this disease and the likely importance of lymphocyte subsets in PKD pathogenesis. Up-regulation of T helper (TH) cell-like response genes and transcription factors implies that T. bryosalmonae may elicit a complex interplay between TH cell subsets. This work, for the first time in the study of fish-myxozoan interactions, suggests that PKD pathogenesis is shaped by an anti-inflammatory phenotype, a profound B cell / antibody response and dysregulated TH cell-like activities. A better understanding of the functional roles of fish immune cells and molecules in PKD pathogenesis may facilitate future development of control measures against this disease.
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