肺吸虫病是一种常见的人畜共患寄生虫病。视黄酸诱导基因I(RIG-I)信号传导对于宿主识别入侵的病原体(尤其是病毒和细菌)非常重要。然而,RIG-I信号在增殖假单胞菌感染早期的作用尚不清楚.因此,在这项研究中,建立Sprague-Dawley(SD)大鼠肺损伤模型。实验方法包括酶联免疫吸附测定(ELISA),实时荧光定量聚合酶链反应(PCR),西方印迹,采用苏木精和伊红(HE)染色,探讨P.prophilus引起肺损伤的机制。因此,RIG-I信号相关关键靶分子的mRNA和蛋白表达,包括RIG-I,肿瘤坏死因子(TNF)受体相关因子6(TRAF6),干扰素调节因子7(IRF7),IPS-1和下游C-X-C趋化因子配体10(CXCL10),感染后立即显著上调,在3或7天达到峰值,14天后呈下降趋势。促炎细胞因子白细胞介素-1(IL-1)的水平,干扰素(IFN)-α,-β,和-γ,代表1型免疫反应,逐渐增加,并在14天达到峰值,这与肺组织HE染色观察到的炎症损伤程度变化相一致。总之,RIG-I信号在增殖假单胞菌感染的早期(14天之前)被激活,由此推断宿主的肺损伤可能与激活RIG-I样信号诱导I型免疫应答有关。
Paragonimiasis is a common zoonotic parasitic disease. The retinoic acid-inducible gene I (RIG-I) signaling is very important for the host to recognize invading pathogens (especially viruses and bacteria). However, the role of RIG-I signaling in the early stages of P. proliferus infection remains unclear. Therefore, in this study, Sprague-Dawley (SD) rat models with lung damage caused by P. proliferus were established. Experimental methods including Enzyme-linked Immuno Sorbent Assay (ELISA), real-time fluorescent quantitative polymerase chain reaction (PCR), western blotting, and hematoxylin and eosin (HE) staining were used to explore the mechanisms of lung injury caused by P. proliferus. As a result, the expression of the mRNA and proteins of RIG-I signal-related key target molecules, including RIG-I, tumor necrosis factor (TNF) receptor associated factor 6 (TRAF6), interferon regulatory Factor 7 (IRF7), IPS-1, and downstream C-X-C chemokine ligand 10 (CXCL10), were significantly up-regulated immediately after infection, peaked at 3 or 7 days, and showed a downward trend on after 14 days. The levels of pro-inflammatory cytokines interleukin-1 (IL-1), interferon (IFN)-α, -β, and -γ, which represent type 1 immune response, gradually increased and reached a peak by 14 days, which was consistent with the changes in the degree of inflammatory damage observed under HE staining of lung tissues. In conclusion, RIG-I signaling is activated in the early stage (before 14 days) of P. proliferus infection, it is inferred that the lung injury of the host may be related to the activation of RIG-I like signaling to induce type I immune response.