伴放线放线杆菌感染对不同组织器官免疫炎症反应的影响
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摘要
目的研究伴放线放线杆菌牙周局部感染和全身感染对正常/高脂饮食新西兰兔组织器官炎症反应的影响，为探讨牙周病与高脂血症相互关系的相关分子生物学机制提供理论依据。
方法实验一：采用高脂饲料喂养6周建立新西兰兔高脂血症模型，兔前磨牙丝线结扎加牙周接种伴放线放线杆菌（Aa）维持8周，建立牙周病模型，分组为A组（ND）：正常饮食，B组（HFD）：高脂饮食，C组（Aa）：局部接种Aa，D组（HFD+Aa）：高脂饮食+局部接种Aa。采用鲎试剂、红外线光谱检测试剂盒提取Aa LPS，55ng/kg注射LPS，一周三次持续8周建立内毒素入血模型。实验二：分组为A组（ND）：正常饮食+注射生理盐水，B组（HFD）：高脂饮食+注射生理盐水，C组（ND+Aa-LPS）：正常饮食+Aa-LPS，D组（HFD+Aa-LPS）：高脂饮食+Aa-LPS，E组（ND+Ec-LPS）：正常饮食+Ec-LPS，F组（HFD+Ec-LPS）：高脂饮食+Ec-LPS。实验动物14周后实施安乐死，取下颌骨做骨丧失的形态学分析；采血测量TC、TG、HDL-C、LDL-C的变化，并用Elisa试剂盒检测兔外周血中CRP、TNF-α、IL-1β、IL-6、IL-10、INF-γ、MCP-1等炎症因子的水平；取主动脉、心肌、肺、肝、肾组织，做HE染色、TNF-α免疫组化染色，采用Realtime-PCR检测组织中TNF-α、IL-1β、CRP、IL-6、IL-10、MMP-9、MCP-1。实验三：实验动物分为四组：A组（ND）：正常饮食，B组（HFD）：高脂饮食，C组（Aa）：注射Aa菌悬液，D组（HFD+Aa）：高脂饮食+注射Aa菌悬液，菌悬液浓度为1.0×108CFU/ml、0.1ml/kg，对照组注射PBS，一周三次持续8周。第14周测量血清中炎症因子。实验四：实验动物建立牙周炎模型后耳源静脉注射IL-10（0.1μg/kg），24h后测量血清中炎症因子。
结果实验一：高脂饮食伴牙周感染的新西兰兔较其他各组动物呈现更高的炎症因子表达和牙槽骨丧失，而且牙周局部Aa感染促进了不同组织器官的病理进程。实验二：全身注射Aa-LPS时，高脂血症动物早期炎症因子表达较正常饮食动物低，而长期慢性Aa-LPS刺激后，高脂饮食新西兰兔其外周血炎症因子和不同组织炎症因子表达均较正常饮食动物高。实验三：长期Aa菌血症感染后，D组动脉粥样硬化程度明显较其他各组高，且各炎症因子表达明显升高。实验四：0.1μg/kg IL-10注射能短暂抑制牙周炎引起的全身反应。
结论Aa局部或全身感染均可上调炎症因子，导致兔血脂代谢紊乱，从而加重高脂血症对组织器官炎症反应。不同组织器官对Aa感染的反应各不相同，Aa感染可能是全身疾病发生发展的危险因素。高脂血症可使机体对细菌感染的敏感性增强并造成免疫失调，表现在早期抗炎和促炎因子的分泌迟钝，以及长期慢性的感染后调整炎症因子的能力下降，分泌量升高。IL-10可短暂抑制牙周炎引起的全身炎症反应。
Objective To investigate the effect of orally or systemically Aggregatibacteractinomycetemcomitans (Aa) infection on the inflammatory response of differenttissue and organs in New Zealand rabbits with normal diet/high-fat diet, and detect thecorrelated molecular mechanism between periodontitis and hyperlipidemia.
Methods Experiment Ⅰ: New Zealand rabbits were fed with the high-fat diet for sixweeks to induce hyperlipemia. Some animals received silk ligatures around theirmandibular premolars followed by an application of Aa for eight weeks, to induceperiodontitis.Animals were divided into four groups, A (ND): normal diet, B (HFD):high-fat diet, C (Aa): local Aa infection, D (HFD+Aa): high-fat diet complicatedwith local Aa infection. Lipopolysaccharide (LPS) isolated from Aa was analyzed byLimulus test and infrared spectroscopy. Rabbits received either repeated intravenousinjections of LPS (55ng/kg, three times per week) for eight weeks. Experiment Ⅱ:Animals were divided into six groups, A (ND): normal diet, B (HFD): high-fat diet, C(Aa-LPS): Aa-LPS injection, D (HFD+Aa-LPS): high-fat diet complicated withAa-LPS injection, E (Ec-LPS): Ec-LPS injection, F (HFD+Ec-LPS): high-fat dietcomplicated with Ec-LPS injection. Animals were carried with euthanasia after14weeks. Periodontal disease severity was quantified radiographically, histologically,and by direct visualization of bone loss. Serum lipids were detected with automaticbiochemistry analyzer and cytokine concentrations were determined usingenzyme-linked immunosorbent assay (ELISA) kits for the assay of rabbit tumornecrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, IL-10and so on. The morphology,mRNA of cytokines in the artery, cardiac, lung, liver, and kidney tissue were investigated by Hematein-Eosin and immununochemistory staining, andRealtime-PCR. Experiment Ⅲ: Animals in experiment I were divided into fourgroups, A (ND): normal diet, B (HFD): high-fat diet, C (Aa): Aa injection, D (HFD+Aa): high-fat diet complicated with Aa injection. The rabbits were treatedintravenously with Aa (1.0×108CFU/ml,0.1ml/kg), or phosphate-buffered salinethree times a week for8weeks and killed at14weeks. The plasma levels of cytokineswere measured. Experiment Ⅳ: Rabbits were induced periodontitis and followed byIL-10(0.1μg/kg) injection. After24hours, the plasma levels of cytokines weremeasured.
Results Experiment Ⅰ: Accompanying pronounced changes in inflammatorycytokine expression was a significantly increase in bone loss for hyperlipidemiarabbits with oral infection with Aa. Local infection of Aa on rabbits accelerated thepathological progression of different organs. Experiment Ⅱ: In the early stages,animals with hyperlipidemia exposed systemically Aa-LPS injection developed ablunted inflammatory response with reduced expression of cytokines compared withnormal diet rabbits. However, rabbits with hyperlipidemia exhibited higherinflammatory cytokine expression for long-term Aa-LPS injection and the rabbitswith HFD have more significance in chronic inflammatory factors expression indifferent organs than those with ND. Experiment Ⅲ: The areas of the aortic sinus thatwere covered with atherosclerotic plaque were significantly larger in Group Dcompared with rabbits from B or C. Aa challenge increased serum CRP, TNF-α,IL-1β, IL-6, IL-10, INF-γ, and MCP-1. Experiment Ⅳ:0.1μg/kg IL-10couldtentatively reduce the expression of periodontitis-induced systemic inflammatoryfactors.
Conclusion Local or systemic infection Aa may lead to the disorder of lipidmetabolism in rabbits, thereby increasing the inflammatory response of differenttissues and organs. The reactions of different organs to Aa infection appearedvariously, infection with Aa might be an additional risk factor for thedevelopment/progression of systemic diseases. HLP becomes associated with a formof immune paralysis and increases susceptibility to other bacterial infections, including an altered pro-and anti-inflammatory network during the acute phase, andmaintaining on a higher expressing level of inflammatory cytokines in the advancedperiod. IL-10could tentatively inhibit the expression of periodontitis-inducedsystemic inflammatory factors.
方法实验一：采用高脂饲料喂养6周建立新西兰兔高脂血症模型，兔前磨牙丝线结扎加牙周接种伴放线放线杆菌（Aa）维持8周，建立牙周病模型，分组为A组（ND）：正常饮食，B组（HFD）：高脂饮食，C组（Aa）：局部接种Aa，D组（HFD+Aa）：高脂饮食+局部接种Aa。采用鲎试剂、红外线光谱检测试剂盒提取Aa LPS，55ng/kg注射LPS，一周三次持续8周建立内毒素入血模型。实验二：分组为A组（ND）：正常饮食+注射生理盐水，B组（HFD）：高脂饮食+注射生理盐水，C组（ND+Aa-LPS）：正常饮食+Aa-LPS，D组（HFD+Aa-LPS）：高脂饮食+Aa-LPS，E组（ND+Ec-LPS）：正常饮食+Ec-LPS，F组（HFD+Ec-LPS）：高脂饮食+Ec-LPS。实验动物14周后实施安乐死，取下颌骨做骨丧失的形态学分析；采血测量TC、TG、HDL-C、LDL-C的变化，并用Elisa试剂盒检测兔外周血中CRP、TNF-α、IL-1β、IL-6、IL-10、INF-γ、MCP-1等炎症因子的水平；取主动脉、心肌、肺、肝、肾组织，做HE染色、TNF-α免疫组化染色，采用Realtime-PCR检测组织中TNF-α、IL-1β、CRP、IL-6、IL-10、MMP-9、MCP-1。实验三：实验动物分为四组：A组（ND）：正常饮食，B组（HFD）：高脂饮食，C组（Aa）：注射Aa菌悬液，D组（HFD+Aa）：高脂饮食+注射Aa菌悬液，菌悬液浓度为1.0×108CFU/ml、0.1ml/kg，对照组注射PBS，一周三次持续8周。第14周测量血清中炎症因子。实验四：实验动物建立牙周炎模型后耳源静脉注射IL-10（0.1μg/kg），24h后测量血清中炎症因子。
结果实验一：高脂饮食伴牙周感染的新西兰兔较其他各组动物呈现更高的炎症因子表达和牙槽骨丧失，而且牙周局部Aa感染促进了不同组织器官的病理进程。实验二：全身注射Aa-LPS时，高脂血症动物早期炎症因子表达较正常饮食动物低，而长期慢性Aa-LPS刺激后，高脂饮食新西兰兔其外周血炎症因子和不同组织炎症因子表达均较正常饮食动物高。实验三：长期Aa菌血症感染后，D组动脉粥样硬化程度明显较其他各组高，且各炎症因子表达明显升高。实验四：0.1μg/kg IL-10注射能短暂抑制牙周炎引起的全身反应。
结论Aa局部或全身感染均可上调炎症因子，导致兔血脂代谢紊乱，从而加重高脂血症对组织器官炎症反应。不同组织器官对Aa感染的反应各不相同，Aa感染可能是全身疾病发生发展的危险因素。高脂血症可使机体对细菌感染的敏感性增强并造成免疫失调，表现在早期抗炎和促炎因子的分泌迟钝，以及长期慢性的感染后调整炎症因子的能力下降，分泌量升高。IL-10可短暂抑制牙周炎引起的全身炎症反应。
Objective To investigate the effect of orally or systemically Aggregatibacteractinomycetemcomitans (Aa) infection on the inflammatory response of differenttissue and organs in New Zealand rabbits with normal diet/high-fat diet, and detect thecorrelated molecular mechanism between periodontitis and hyperlipidemia.
Methods Experiment Ⅰ: New Zealand rabbits were fed with the high-fat diet for sixweeks to induce hyperlipemia. Some animals received silk ligatures around theirmandibular premolars followed by an application of Aa for eight weeks, to induceperiodontitis.Animals were divided into four groups, A (ND): normal diet, B (HFD):high-fat diet, C (Aa): local Aa infection, D (HFD+Aa): high-fat diet complicatedwith local Aa infection. Lipopolysaccharide (LPS) isolated from Aa was analyzed byLimulus test and infrared spectroscopy. Rabbits received either repeated intravenousinjections of LPS (55ng/kg, three times per week) for eight weeks. Experiment Ⅱ:Animals were divided into six groups, A (ND): normal diet, B (HFD): high-fat diet, C(Aa-LPS): Aa-LPS injection, D (HFD+Aa-LPS): high-fat diet complicated withAa-LPS injection, E (Ec-LPS): Ec-LPS injection, F (HFD+Ec-LPS): high-fat dietcomplicated with Ec-LPS injection. Animals were carried with euthanasia after14weeks. Periodontal disease severity was quantified radiographically, histologically,and by direct visualization of bone loss. Serum lipids were detected with automaticbiochemistry analyzer and cytokine concentrations were determined usingenzyme-linked immunosorbent assay (ELISA) kits for the assay of rabbit tumornecrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, IL-10and so on. The morphology,mRNA of cytokines in the artery, cardiac, lung, liver, and kidney tissue were investigated by Hematein-Eosin and immununochemistory staining, andRealtime-PCR. Experiment Ⅲ: Animals in experiment I were divided into fourgroups, A (ND): normal diet, B (HFD): high-fat diet, C (Aa): Aa injection, D (HFD+Aa): high-fat diet complicated with Aa injection. The rabbits were treatedintravenously with Aa (1.0×108CFU/ml,0.1ml/kg), or phosphate-buffered salinethree times a week for8weeks and killed at14weeks. The plasma levels of cytokineswere measured. Experiment Ⅳ: Rabbits were induced periodontitis and followed byIL-10(0.1μg/kg) injection. After24hours, the plasma levels of cytokines weremeasured.
Results Experiment Ⅰ: Accompanying pronounced changes in inflammatorycytokine expression was a significantly increase in bone loss for hyperlipidemiarabbits with oral infection with Aa. Local infection of Aa on rabbits accelerated thepathological progression of different organs. Experiment Ⅱ: In the early stages,animals with hyperlipidemia exposed systemically Aa-LPS injection developed ablunted inflammatory response with reduced expression of cytokines compared withnormal diet rabbits. However, rabbits with hyperlipidemia exhibited higherinflammatory cytokine expression for long-term Aa-LPS injection and the rabbitswith HFD have more significance in chronic inflammatory factors expression indifferent organs than those with ND. Experiment Ⅲ: The areas of the aortic sinus thatwere covered with atherosclerotic plaque were significantly larger in Group Dcompared with rabbits from B or C. Aa challenge increased serum CRP, TNF-α,IL-1β, IL-6, IL-10, INF-γ, and MCP-1. Experiment Ⅳ:0.1μg/kg IL-10couldtentatively reduce the expression of periodontitis-induced systemic inflammatoryfactors.
Conclusion Local or systemic infection Aa may lead to the disorder of lipidmetabolism in rabbits, thereby increasing the inflammatory response of differenttissues and organs. The reactions of different organs to Aa infection appearedvariously, infection with Aa might be an additional risk factor for thedevelopment/progression of systemic diseases. HLP becomes associated with a formof immune paralysis and increases susceptibility to other bacterial infections, including an altered pro-and anti-inflammatory network during the acute phase, andmaintaining on a higher expressing level of inflammatory cytokines in the advancedperiod. IL-10could tentatively inhibit the expression of periodontitis-inducedsystemic inflammatory factors.
引文
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