旋毛虫排泄分泌物调节巨噬细胞及成肌细胞功能的体外研究
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摘要
旋毛虫是一种寄生于宿主骨骼肌细胞内的胞内寄生线虫,感染所有的哺乳动物(包括人类)和一些食肉鸟类。旋毛虫病是由旋毛虫(Trichinella)引起的一种呈全球性分布的食源性人兽共患寄生虫病。人类旋毛虫病在许多国家爆发,目前在世界范围内约有1100万人被感染,在我国该病仍有发生。旋毛虫感染不同于其他线虫,他的生活史在单一宿主内完成,分成三个主要阶段:成虫、新生幼虫和肌幼虫,其分别寄生于宿主肠上皮细胞和骨骼肌细胞。旋毛虫在感染不同时期,释放许多生物活性物质调节宿主免疫反应并入侵宿主肌细胞为自己构建了一个安全的家(包囊)来达到成功的寄生。
在宿主抵抗外来病原入侵的免疫应答过程中,巨噬细胞在起始,调节,终末效应的各个环节起着重要的作用,因此他被认为是参与机体免疫应答的主要细胞。巨噬细胞在线虫感染中,已作为寄生虫调节宿主免疫反应的靶细胞,对寄生虫生存具有重要意义。另外,巨噬细胞在肌肉损伤的修复过程中也扮演着重要的角色,他不仅可以吞噬凋亡坏死的细胞碎片,而且通过其释放的活性因子调节卫星细胞的激活与分化。目前关于旋毛虫排泄分泌物(即ES)对肌细胞及巨噬细胞功能影响的报道比较少,研究不同时期ES产物对这些细胞功能的影响将有利于我们进一步的阐明旋毛虫免疫逃逸及包囊形成机制。
首先,本研究选择了小鼠巨噬细胞系J774A.1做为细胞模型,调查了旋毛虫不同时期ES产物对巨噬细胞活性的影响。SYBR Green I实时荧光定量PCR和ELISA结果表明,不同时期ES产物降低了LPS刺激的巨噬细胞分泌促炎性细胞因子(IL-1β、IL-12、TNF-α和IL-6)的能力。然而只有旋毛虫3日龄成虫排泄分泌物(AD3 ES)和旋毛虫5日龄成虫(AD5)与新生幼虫(NBL)混合排泄分泌物(AD5-NBL ES)明显抑制了LPS刺激的效应分子iNOS的表达。我们发现:在ES产物单独作用组,旋毛虫不同时期ES产物上调了抗炎性细胞因子(IL-10和TGF-β)和替代性活化的巨噬细胞标记物Arg1的表达,相反抑制了iNOS的表达,因此我们推测ES产物可能调节巨噬细胞向可替代激活表型转化。另外我们通过细胞免疫荧光和Western blot技术分别检测了NF-κB信号通路中NF-κB的核易位以及MAPKs信号通路的磷酸化情况。结果表明,旋毛虫不同时期ES产物至少部分依靠这两条信号传导通路来抑制促炎性细胞因子的表达。我们推测旋毛虫可以通过抑制促炎性细胞因子的产生和诱导巨噬细胞向可替代激活表型的转换,在巨噬细胞水平调节宿主免疫反应,这将有利于旋毛虫的生存和宿主健康。
其次,本研究将肌幼虫期排泄分泌物(ML ES)体外作用于小鼠C2C12成肌细胞,采用CCK-8、SYBR Green I实时荧光定量PCR、细胞免疫荧光和Western blot检测ML ES对成肌分化程序的影响。CCK-8分析表明,在低血清条件下,ML ES促进成肌细胞的增殖,同时细胞免疫荧光和Western blot结果表明,在分化条件下,ML ES增强C2C12成肌细胞的细胞增殖核抗原(PCNA)和细胞周期调节因子cyclin D1的表达。另外我们检测了肌细胞终末分化标记物肌球蛋白重链(MHC)的表达,结果显示ML ES作用的成肌细胞MHC的转录及表达明显下降,表明ML ES抑制了C2C12成肌细胞的分化,进一步的细胞免疫荧光实验表明这一抑制效应是可以逆转的。同时,我们调查了抑制机制,结果表明ML ES在转录和转录后水平抑制细胞分化相关因子(MyoD、Myogenin、p21)的表达和p38 MAPK的磷酸化水平。这些结果表明ML ES中存在重要的调节因子能够促使成肌细胞的增殖但抑制它的分化。
最后我们利用共培养技术,建立了巨噬细胞与成肌细胞共培养模型,在体外调查了与旋毛虫ML ES作用后的巨噬细胞共培养对成肌细胞分化的影响。我们的结果表明成肌细胞与ML ES作用后的巨噬细胞共培养上调了成肌细胞PCNA和cyclin D1的表达,说明ML ES作用后的巨噬细胞可以增强成肌细胞的增殖。另外细胞免疫荧光表明,与对照组比较,成肌细胞分化调节因子(MyoD、Myogenin、p21)阳性细胞的数量及终末分化标记物MHC的表达明显降低。我们进一步用Western blot验证了这种抑制效果。本研究表明旋毛虫ML ES不仅可以直接调节成肌细胞的分化,而且可以通过调节巨噬细胞活性来影响成肌细胞的分化,这为研究旋毛虫与宿主细胞及旋毛虫感染后,宿主细胞间相互对话的复杂机制提供了新的思路。
Trichinella spiralis is an intracellular parasite of skeletal muscle, which can infect a wide variety of mammalian species and some carnivorous birds. Trichinellosis is a widespread food-borne zoonosis. Human trichinellosis outbreaks occur in many parts of the world, and it has been estimated that as many as 11 million people are infected with Trichinella. There is still a high prevalence in China. Trichinella differs from other helminthes because its life cycle which is reproduced in the same host involves two distinct intracellular habitats, intestianal epithelium and skeletal cell and can be divided into three main stages: adult worms, newborn larvae, and muscle larvae. During the infection, T. spiralis release a variety of biologically active proteins to regulate host immune and invasive the muscle cell to construct their home, named nurse cell, which are very important to parasitize successfully.
Macrophages play crucial roles in the immune response agaist infections, as they can initiate, modulate and also be final effector cells during immune responses. During helminth infections, macrophages, the important targets for immunomodulation, have been shown to play a central role in helminth survival. Moreover, macrophages play an important role in repairing injured muscle, which do not only play important role as scavengers to clear cell debris, but also can regulate satellite cell proliferation and differentiation by releasing some active factors. Now, how ES products modulate macrophage and muscle cell functions as well as signal transduction pathways is largely unknown. Research on the impact of different stages of ES products on these host cell function will be benefical for us to clarify the mechanism of immune evasion and nurse cell formation.
First of all, we investigated the effect of ES products from different stages of T. spiralis on modulating J774A.1 macrophage activities. The ELISA and real-time PCR results indicated that ES products from different stages of T. spiralis reduced the capacity of macrophages to express pro-inflammatory cytokines (tumor necrosis factor (TNF-α), interleukin-1β(IL-1β), interleukin-6 (IL-6), and interleukin-12 (IL-12)) in response to lipopolysaccharide (LPS) challenge. However, only ES products from 3-day-old adult worms (AD3) and 5-day-old adult worms/newborn larvae (AD5-NBL) significantly inhibited inducible nitric oxide synthase (iNOS) gene expression in LPS-induced macrophages. In addition, ES products from different stages of T. spiralis alone boosted the expression of anti-inflammatory cytokines interleukin-10 (IL-10) and transforming growth factor-β(TGF-β) and effector molecule arginase 1 (Arg1) in J774A.1 macrophages. In contrast, ES products alone reduced iNOS expression. Signal transduction studies showed that ES products significantly inhibited nuclear factor-κB (NF-κB) translocation into the nucleus and the phosphorylation of both extracellular signal-regulated protein kinase 1/2 (ERK1/2) and p38 mitogen-activated protein kinase (p38 MAPK) in LPS-stimulated J774A.1 macrophages. Therefore, we hypothesize that during T. spiralis infection, ES products least partly depend on inhibiting these pathway to suppress pro-inflammatory products. These results suggest that ES products regulate host immune response at the macrophage level, which may be important for worm survival and host health. Secondly, utilizing a C2C12 myoblast cell line, the ability of ES from muscle larvae of T. spiralis to influence proliferation and differentiation of murine myoblasts was evaluated in vitro by CCK-8, real-time PCR, immunofluorescence and western-blot technique. CCK-8 results showed that ML ES products significantly enhance cell proliferation under low-serum conditions and dose-dependent manner. Moreover, immunofluorescence and western-blot analysis demonstrated that in differentiation condition, ML ES increase the PCNA and cyclin D1 expression, compared with control group. In addition, our biochemical analysis showed that ML ES reduce the expression of MHC in transcription and post transcription, a marker of sarcomere assembley during terminal differentiation. This result suggests that ML ES reversibly inhibited their differentiation. Furthermore, we exam the mechamism by which ML ES inhibit C2C12 myoblast differentiation, the results showed that ML ES inhibitd the expression of MRFs (MyoD and Myogenin), as well as p21 expression. ML ES also suppressed the phophoryation of p38 MAPK in C2C12 myoblast. Take together, these results imply that some important mediators in ML ES are able to
promote proliferation but inhibit differentiation in murine skeletal myoblast, which provide an important insight for full understanding of the mechanisms of T. spiralis to induce infected muscle cell phenotype change and nurse cell formation.
Finally, we investigated the effect of ML ES-treated macrophage on C2C12 myoblasts differentiation program in vitro using the co-culture technique. In the treated group, increase expression of PCNA and cyclin D1 indicated that cocultured ML ES-treated macrophages enhance the C2C12 myoblast proliferation. In contrast, the immunostaining showed that the expression of MRFs (MyoD and Myogenin), p21 and MHC were reduced as compared with control group, indicating that cocultured ML ES-treated macrophages inhibit myoblasts differentiation. The inhibitory effects of ML ES on the expression MRFs (MyoD and Myogenin) and MHC were confirmed by western-blot analysis. Our study showed that ML ES not only directly regulate myoblast differentiation, but also can indirectly influence myoblasts differentiation by regulating macrophages activity, which provide new opinion for elucidate complex mechanism of cell-parasite and cell-cell interaction during T. spiralis infection.
在宿主抵抗外来病原入侵的免疫应答过程中,巨噬细胞在起始,调节,终末效应的各个环节起着重要的作用,因此他被认为是参与机体免疫应答的主要细胞。巨噬细胞在线虫感染中,已作为寄生虫调节宿主免疫反应的靶细胞,对寄生虫生存具有重要意义。另外,巨噬细胞在肌肉损伤的修复过程中也扮演着重要的角色,他不仅可以吞噬凋亡坏死的细胞碎片,而且通过其释放的活性因子调节卫星细胞的激活与分化。目前关于旋毛虫排泄分泌物(即ES)对肌细胞及巨噬细胞功能影响的报道比较少,研究不同时期ES产物对这些细胞功能的影响将有利于我们进一步的阐明旋毛虫免疫逃逸及包囊形成机制。
首先,本研究选择了小鼠巨噬细胞系J774A.1做为细胞模型,调查了旋毛虫不同时期ES产物对巨噬细胞活性的影响。SYBR Green I实时荧光定量PCR和ELISA结果表明,不同时期ES产物降低了LPS刺激的巨噬细胞分泌促炎性细胞因子(IL-1β、IL-12、TNF-α和IL-6)的能力。然而只有旋毛虫3日龄成虫排泄分泌物(AD3 ES)和旋毛虫5日龄成虫(AD5)与新生幼虫(NBL)混合排泄分泌物(AD5-NBL ES)明显抑制了LPS刺激的效应分子iNOS的表达。我们发现:在ES产物单独作用组,旋毛虫不同时期ES产物上调了抗炎性细胞因子(IL-10和TGF-β)和替代性活化的巨噬细胞标记物Arg1的表达,相反抑制了iNOS的表达,因此我们推测ES产物可能调节巨噬细胞向可替代激活表型转化。另外我们通过细胞免疫荧光和Western blot技术分别检测了NF-κB信号通路中NF-κB的核易位以及MAPKs信号通路的磷酸化情况。结果表明,旋毛虫不同时期ES产物至少部分依靠这两条信号传导通路来抑制促炎性细胞因子的表达。我们推测旋毛虫可以通过抑制促炎性细胞因子的产生和诱导巨噬细胞向可替代激活表型的转换,在巨噬细胞水平调节宿主免疫反应,这将有利于旋毛虫的生存和宿主健康。
其次,本研究将肌幼虫期排泄分泌物(ML ES)体外作用于小鼠C2C12成肌细胞,采用CCK-8、SYBR Green I实时荧光定量PCR、细胞免疫荧光和Western blot检测ML ES对成肌分化程序的影响。CCK-8分析表明,在低血清条件下,ML ES促进成肌细胞的增殖,同时细胞免疫荧光和Western blot结果表明,在分化条件下,ML ES增强C2C12成肌细胞的细胞增殖核抗原(PCNA)和细胞周期调节因子cyclin D1的表达。另外我们检测了肌细胞终末分化标记物肌球蛋白重链(MHC)的表达,结果显示ML ES作用的成肌细胞MHC的转录及表达明显下降,表明ML ES抑制了C2C12成肌细胞的分化,进一步的细胞免疫荧光实验表明这一抑制效应是可以逆转的。同时,我们调查了抑制机制,结果表明ML ES在转录和转录后水平抑制细胞分化相关因子(MyoD、Myogenin、p21)的表达和p38 MAPK的磷酸化水平。这些结果表明ML ES中存在重要的调节因子能够促使成肌细胞的增殖但抑制它的分化。
最后我们利用共培养技术,建立了巨噬细胞与成肌细胞共培养模型,在体外调查了与旋毛虫ML ES作用后的巨噬细胞共培养对成肌细胞分化的影响。我们的结果表明成肌细胞与ML ES作用后的巨噬细胞共培养上调了成肌细胞PCNA和cyclin D1的表达,说明ML ES作用后的巨噬细胞可以增强成肌细胞的增殖。另外细胞免疫荧光表明,与对照组比较,成肌细胞分化调节因子(MyoD、Myogenin、p21)阳性细胞的数量及终末分化标记物MHC的表达明显降低。我们进一步用Western blot验证了这种抑制效果。本研究表明旋毛虫ML ES不仅可以直接调节成肌细胞的分化,而且可以通过调节巨噬细胞活性来影响成肌细胞的分化,这为研究旋毛虫与宿主细胞及旋毛虫感染后,宿主细胞间相互对话的复杂机制提供了新的思路。
Trichinella spiralis is an intracellular parasite of skeletal muscle, which can infect a wide variety of mammalian species and some carnivorous birds. Trichinellosis is a widespread food-borne zoonosis. Human trichinellosis outbreaks occur in many parts of the world, and it has been estimated that as many as 11 million people are infected with Trichinella. There is still a high prevalence in China. Trichinella differs from other helminthes because its life cycle which is reproduced in the same host involves two distinct intracellular habitats, intestianal epithelium and skeletal cell and can be divided into three main stages: adult worms, newborn larvae, and muscle larvae. During the infection, T. spiralis release a variety of biologically active proteins to regulate host immune and invasive the muscle cell to construct their home, named nurse cell, which are very important to parasitize successfully.
Macrophages play crucial roles in the immune response agaist infections, as they can initiate, modulate and also be final effector cells during immune responses. During helminth infections, macrophages, the important targets for immunomodulation, have been shown to play a central role in helminth survival. Moreover, macrophages play an important role in repairing injured muscle, which do not only play important role as scavengers to clear cell debris, but also can regulate satellite cell proliferation and differentiation by releasing some active factors. Now, how ES products modulate macrophage and muscle cell functions as well as signal transduction pathways is largely unknown. Research on the impact of different stages of ES products on these host cell function will be benefical for us to clarify the mechanism of immune evasion and nurse cell formation.
First of all, we investigated the effect of ES products from different stages of T. spiralis on modulating J774A.1 macrophage activities. The ELISA and real-time PCR results indicated that ES products from different stages of T. spiralis reduced the capacity of macrophages to express pro-inflammatory cytokines (tumor necrosis factor (TNF-α), interleukin-1β(IL-1β), interleukin-6 (IL-6), and interleukin-12 (IL-12)) in response to lipopolysaccharide (LPS) challenge. However, only ES products from 3-day-old adult worms (AD3) and 5-day-old adult worms/newborn larvae (AD5-NBL) significantly inhibited inducible nitric oxide synthase (iNOS) gene expression in LPS-induced macrophages. In addition, ES products from different stages of T. spiralis alone boosted the expression of anti-inflammatory cytokines interleukin-10 (IL-10) and transforming growth factor-β(TGF-β) and effector molecule arginase 1 (Arg1) in J774A.1 macrophages. In contrast, ES products alone reduced iNOS expression. Signal transduction studies showed that ES products significantly inhibited nuclear factor-κB (NF-κB) translocation into the nucleus and the phosphorylation of both extracellular signal-regulated protein kinase 1/2 (ERK1/2) and p38 mitogen-activated protein kinase (p38 MAPK) in LPS-stimulated J774A.1 macrophages. Therefore, we hypothesize that during T. spiralis infection, ES products least partly depend on inhibiting these pathway to suppress pro-inflammatory products. These results suggest that ES products regulate host immune response at the macrophage level, which may be important for worm survival and host health. Secondly, utilizing a C2C12 myoblast cell line, the ability of ES from muscle larvae of T. spiralis to influence proliferation and differentiation of murine myoblasts was evaluated in vitro by CCK-8, real-time PCR, immunofluorescence and western-blot technique. CCK-8 results showed that ML ES products significantly enhance cell proliferation under low-serum conditions and dose-dependent manner. Moreover, immunofluorescence and western-blot analysis demonstrated that in differentiation condition, ML ES increase the PCNA and cyclin D1 expression, compared with control group. In addition, our biochemical analysis showed that ML ES reduce the expression of MHC in transcription and post transcription, a marker of sarcomere assembley during terminal differentiation. This result suggests that ML ES reversibly inhibited their differentiation. Furthermore, we exam the mechamism by which ML ES inhibit C2C12 myoblast differentiation, the results showed that ML ES inhibitd the expression of MRFs (MyoD and Myogenin), as well as p21 expression. ML ES also suppressed the phophoryation of p38 MAPK in C2C12 myoblast. Take together, these results imply that some important mediators in ML ES are able to
promote proliferation but inhibit differentiation in murine skeletal myoblast, which provide an important insight for full understanding of the mechanisms of T. spiralis to induce infected muscle cell phenotype change and nurse cell formation.
Finally, we investigated the effect of ML ES-treated macrophage on C2C12 myoblasts differentiation program in vitro using the co-culture technique. In the treated group, increase expression of PCNA and cyclin D1 indicated that cocultured ML ES-treated macrophages enhance the C2C12 myoblast proliferation. In contrast, the immunostaining showed that the expression of MRFs (MyoD and Myogenin), p21 and MHC were reduced as compared with control group, indicating that cocultured ML ES-treated macrophages inhibit myoblasts differentiation. The inhibitory effects of ML ES on the expression MRFs (MyoD and Myogenin) and MHC were confirmed by western-blot analysis. Our study showed that ML ES not only directly regulate myoblast differentiation, but also can indirectly influence myoblasts differentiation by regulating macrophages activity, which provide new opinion for elucidate complex mechanism of cell-parasite and cell-cell interaction during T. spiralis infection.
引文
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