發(fā)布時間：2018-07-03 15:01

  本文選題：Toll樣受體2 + 脂磷壁酸　； 參考：《安徽醫(yī)科大學(xué)》2016年博士論文

【摘要】：TAM受體-Tyro3、Axl和Mer,組成受體酪氨酸激酶(RTK)一個獨特的亞家族,為單次跨膜蛋白。TAM受體通過二大基本生物學(xué)功能(凋亡細(xì)胞的吞噬和先天性炎癥免疫反應(yīng)的抑制)來維護體內(nèi)免疫內(nèi)環(huán)境穩(wěn)定。我們在本論文中主要針對Mer受體酪氨酸激酶(Mer TK)在脂磷壁酸(LTA)誘導(dǎo)炎癥反應(yīng)調(diào)控和金葡菌吞噬中的作用進行研究。一.Mer TK調(diào)控脂磷壁酸(LTA)誘導(dǎo)炎癥反應(yīng)的分子機制研究研究背景LTA和LPS分別代表嵌入在革蘭氏陽性菌和革蘭氏陰性菌細(xì)胞壁的二個主要的PAMP分子。目前,有研究證實Mer TK負(fù)性調(diào)控LPS誘導(dǎo)的炎癥反應(yīng)。然而,在LTA誘導(dǎo)的炎癥反應(yīng)中,Mer TK是否具有類似的作用及其潛在機制仍有待于闡明。研究目的1.LTA刺激RAW264.7巨噬細(xì)胞,研究TLR2促炎信號和Mer TK抗炎信號相關(guān)蛋白的表達。2.探討Mer TK信號在LTA刺激RAW264.7巨噬細(xì)胞所誘導(dǎo)炎癥反應(yīng)中的作用及其潛在機制。研究方法1.Western Blot檢測LTA刺激巨噬細(xì)胞中相關(guān)蛋白的表達用LTA在不同時間點(4h、8h、12h、24h)刺激小鼠單核巨噬細(xì)胞RAW264.7。采用Western Blot方法檢測TLR2信號和Mer TK信號相關(guān)蛋白分子的表達水平。2.Gas6中和抗體對LTA誘導(dǎo)Mer TK活化的影響首先,使用特異性Mer抑制抗體預(yù)處理RAW264.7巨噬細(xì)胞1h后,分別用200 ng/ml LTA刺激RAW264.7細(xì)胞12h及400 ng/ml Gas6刺激RAW264.7細(xì)胞10 min。其次,使用Gas6中和抗體預(yù)處理RAW264.7巨噬細(xì)胞1h后,用200 ng/ml LTA刺激RAW264.7細(xì)胞12h。最后都通過Western Blot方法檢測Mer TK活化情況。3.采用免疫細(xì)胞化學(xué)和Western Blot方法檢測靶向干預(yù)Mer TK后Mer TK and P-Mer TK的表達使用特異性Mer抑制抗體或Ig G預(yù)處理RAW264.7巨噬細(xì)胞1h,再用200 ng/ml LTA刺激RAW264.7細(xì)胞12h,然后分別采用免疫細(xì)胞化學(xué)和Western Blot方法檢測Mer TK and P-Mer TK的表達水平。4.靶向干預(yù)Mer TK對LTA誘導(dǎo)炎癥反應(yīng)及TLR2和Mer TK信號下游相關(guān)蛋白表達的影響首先,使用特異性Mer抑制抗體或Ig G預(yù)處理RAW264.7巨噬細(xì)胞1h,再用200ng/ml LTA刺激RAW264.7細(xì)胞48h,然后采用ELISA方法檢測培養(yǎng)上清中促炎癥因子TNF-αand IL-6的表達水平。其次,使用特異性Mer抑制抗體預(yù)處理RAW264.7巨噬細(xì)胞1h,再用200 ng/ml LTA刺激RAW264.7細(xì)胞12h,然后采用Western Blot方法檢測TLR2信號和Mer TK信號下游相關(guān)蛋白分子的表達水平變化。5.靶向抑制PI3K對LTA誘導(dǎo)炎癥反應(yīng)及TLR2信號下游相關(guān)蛋白表達的影響首先,使用PI3K特異性抑制劑LY294002預(yù)處理RAW264.7巨噬細(xì)胞1h,再用200ng/ml LTA刺激RAW264.7細(xì)胞48h,然后采用ELISA方法檢測培養(yǎng)上清中促炎癥因子TNF-αand IL-6的表達水平。其次,使用PI3K特異性抑制劑LY294002預(yù)處理RAW264.7巨噬細(xì)胞1h,再用200 ng/ml LTA刺激RAW264.7細(xì)胞12h,然后采用Western Blot方法檢測TLR2信號下游相關(guān)蛋白分子的表達水平變化。研究結(jié)果1.LTA刺激巨噬細(xì)胞能夠活化TLR2信號通路和Mer TK信號通路RAW264.7細(xì)胞在LTA刺激作用下,TLR2信號通路下游相關(guān)蛋白分子My D88、IκB-α、p65及ERK被活化;此外,Mer TK信號通路下游相關(guān)蛋白分子Akt和SOCS3也被活化。而且,除了ERK之外它們的活化是呈現(xiàn)時間依賴性方式。2.LTA誘導(dǎo)Mer TK活化是Gas6依賴性的首先,使用特異性Mer抑制抗體預(yù)處理能顯著降低LTA以及Gas6刺激RAW264.7細(xì)胞誘導(dǎo)的Mer TK磷酸化水平。其次,使用Gas6中和抗體預(yù)處理能明顯抑制LTA誘導(dǎo)的Mer TK的活化。3.Mer TK負(fù)性調(diào)控LTA誘導(dǎo)的炎癥反應(yīng)使用特異性Mer抑制抗體預(yù)處理能明顯增加LTA刺激RAW264.7細(xì)胞誘導(dǎo)促炎癥因子TNF-α和IL-6的水平。而且,使用特異性Mer抑制抗體預(yù)處理能明顯增強NF-κB的活化(P-IκB-α、P-p65表達水平明顯升高)。4.Mer TK通過PI3K/Akt信號通路和SOCS3蛋白參與LTA誘導(dǎo)炎癥反應(yīng)的負(fù)調(diào)控RAW264.7細(xì)胞在LTA刺激作用下,Akt和SOCS3活化是Mer TK依賴性的。同時,使用特異性Mer抑制抗體預(yù)處理能明顯阻止LTA誘導(dǎo)的Akt和SOCS3活化;而且PI3K/Akt通路和SOCS3蛋白抑制TLR2介導(dǎo)的炎癥反應(yīng)。研究結(jié)論1.LTA刺激巨噬細(xì)胞誘導(dǎo)了TLR2促炎信號和Mer TK抗炎信號通路的活化。2.Mer TK通過PI3K/Akt通路和SOCS3蛋白來負(fù)性調(diào)控LTA所誘導(dǎo)的炎癥反應(yīng)。二.Mer TK在巨噬細(xì)胞吞噬金葡菌中的作用研究研究背景目前,研究證明表達于巨噬細(xì)胞表面的許多受體同時參與凋亡細(xì)胞和細(xì)菌的識別與吞噬,包括SR-A、CD14、整合素、補體受體和Fc受體等。此外,表達于巨噬細(xì)胞表面的Mer TK對于凋亡細(xì)胞的迅速吞噬是必不可少的。因此,本研究我們探討Mer TK受體是否也參與對細(xì)菌的吞噬。研究目的1.金葡菌刺激RAW264.7巨噬細(xì)胞,檢測吞噬信號相關(guān)蛋白的表達。2.研究Mer TK在RAW264.7巨噬細(xì)胞吞噬金葡菌中的作用。研究方法1.Western Blot檢測金葡菌刺激巨噬細(xì)胞中相關(guān)蛋白的表達用金葡菌在不同時間(20min、40min、60min、120min)刺激RAW264.7巨噬細(xì)胞。然后,采用Western Blot方法檢測在金葡菌刺激RAW264.7巨噬細(xì)胞過程中相關(guān)蛋白分子的表達水平。2.分別從蛋白分子水平和形態(tài)學(xué)方面研究Mer TK對巨噬細(xì)胞吞噬金葡菌的影響我們從蛋白分子水平檢測Mer TK對RAW264.7巨噬細(xì)胞吞噬相關(guān)蛋白分子的影響。使用特異性Mer抑制抗體預(yù)處理RAW264.7巨噬細(xì)胞1h,再用金葡菌刺激RAW264.7細(xì)胞1h后。首先,通過Western Blot方法檢測吞噬相關(guān)蛋白P-FAK及GTP-Rac1的表達水平。其次,通過吞噬試驗對RAW264.7細(xì)胞的吞噬金葡菌的能力進行評估。研究結(jié)果1.金葡菌刺激RAW264.7細(xì)胞能夠引起其表面多種受體分子的活化金葡菌刺激RAW264.7細(xì)胞能夠引起其表面多種受體分子的活化,包括TLR2信號通路(My D88、p65、JNK、ERK、p38)、SR-A及Mer TK,并且它們的活化呈時間依賴性方式。2.金葡菌刺激RAW264.7細(xì)胞能夠誘導(dǎo)吞噬相關(guān)蛋白FAK及Rac1的活化同時,金葡菌刺激RAW264.7細(xì)胞能夠引起FAK磷酸化水平明顯的增加以及體現(xiàn)Rac1活化的GTP-Rac1表達水平的增高,并且也呈時間依賴性方式。3.靶向干預(yù)Mer TK對金葡菌誘導(dǎo)FAK及Rac1的活化無明顯影響使用特異性Mer抑制抗體預(yù)處理RAW264.7巨噬細(xì)胞1h,再用金葡菌刺激RAW264.7細(xì)胞1h,之后我們從蛋白分子水平檢測了這種特異性Mer抑制抗體對吞噬信號通路相關(guān)蛋白P-FAK及GTP-Rac1的影響。我們發(fā)現(xiàn),這種抗體對金葡菌刺激RAW264.7細(xì)胞活化的P-FAK和GTP-Rac1的表達水平無明顯影響。4.Mer TK對巨噬細(xì)胞吞噬金葡菌的能力無顯著影響為了進一步證實Mer TK在巨噬細(xì)胞吞噬金葡菌中的作用,我們通過吞噬試驗對RAW264.7巨噬細(xì)胞的吞噬金葡菌的能力進行評估。我們發(fā)現(xiàn),給予特異性Mer抑制抗體預(yù)處理后,RAW264.7細(xì)胞吞噬金葡菌的能力無顯著性變化。研究結(jié)論1.金葡菌刺激巨噬細(xì)胞誘導(dǎo)吞噬信號及Mer TK的活化。2.然而,Mer TK對巨噬細(xì)胞吞噬金葡菌不是重要的。
[Abstract]:TAM receptor -Tyro3, Axl and Mer, which constitute a unique subfamily of receptor tyrosine kinase (RTK), maintain the internal immune stability in the body by two basic biological functions (the phagocytosis of apoptotic cells and innate inflammatory immune response) for the single transmembrane protein.TAM receptor. In this paper, we mainly focus on the Mer receptor tyrosine. The role of kinase (Mer TK) in the regulation of inflammatory response induced by lipophosphoric acid (LTA) and the role of Staphylococcus aureus phagocytosis. A molecular mechanism for the regulation of lipophosphoric acid (LTA) induced inflammatory response by.Mer TK; background LTA and LPS represent two major PAMP molecules embedded in gram positive bacteria and gram negative bacteria cell walls respectively. Studies have confirmed that Mer TK negatively regulates the inflammatory response induced by LPS. However, in the case of LTA induced inflammatory reactions, whether Mer TK has a similar role and its potential mechanism remains to be clarified. The purpose of the study is to stimulate RAW264.7 macrophages and to study the expression of the TLR2 proinflammatory signal and Mer TK anti-inflammatory signal related proteins. The role of TA to stimulate the inflammatory response induced by RAW264.7 macrophages. Methods 1.Western Blot was used to detect the expression of related proteins in macrophages stimulated by LTA and LTA at different time points (4h, 8h, 12h, 24h) stimulated the mononuclear macrophages in mice. The effect of.2.Gas6 neutralization antibody on the activation of Mer TK induced by LTA first. After using specific Mer to pretreat RAW264.7 macrophage 1H, 200 ng/ml LTA stimulates RAW264.7 cell 12h and 400 ng/ml to stimulate 10. Then, the RAW264.7 cell 12h. was stimulated by 200 ng/ml LTA and the activation of Mer TK was detected by Western Blot method. AW264.7 cells 12h, and then using immunocytochemistry and Western Blot method to detect the expression level of Mer TK and P-Mer TK.4. target intervention Mer TK to induce inflammatory response and the expression of downstream related proteins. Ng/ml LTA stimulates RAW264.7 cell 48h, and then uses ELISA method to detect the expression level of TNF- alpha and IL-6 in culture supernatant. Secondly, using specific Mer inhibition antibody preconditioning RAW264.7 macrophage 1H, then 200 ng/ml stimuli are used to stimulate the cells. Changes in the expression level of the associated protein molecules.5. targeting inhibition of PI3K on LTA induced inflammatory response and the expression of downstream related proteins in TLR2 signals first, PI3K specific inhibitor LY294002 pretreated RAW264.7 macrophage 1H, and then 200ng/ml LTA stimulated RAW264.7 cell 48h, and then used to detect proinflammatory in culture supernatant. The expression level of TNF- alpha and IL-6. Second, RAW264.7 macrophage 1H was pretreated with PI3K specific inhibitor LY294002, and RAW264.7 cell 12h was stimulated with 200 ng/ml LTA. 2 signal pathway and Mer TK signaling pathway RAW264.7 cells are activated by LTA, the downstream related protein molecules of the TLR2 signaling pathway, My D88, I kappa B- alpha, p65 and ERK are activated. Besides, the downstream related protein molecules of the Mer signaling pathway are also activated. Besides, the activation of the downstream related proteins in the Mer signaling pathway is also activated in a time dependent manner. TK activation is the first of Gas6 dependence. The use of specific Mer inhibition antibody preconditioning can significantly reduce the level of Mer TK phosphorylation induced by LTA and Gas6 stimulation of RAW264.7 cells. Secondly, the use of Gas6 neutralization antibody preconditioning can significantly inhibit the activation of Mer TK induced by LTA. Antibody preconditioning can significantly increase the level of LTA stimulated RAW264.7 cells to induce TNF- alpha and IL-6. Moreover, the activation of NF- kappa B can be significantly enhanced by specific Mer inhibition antibody preconditioning (P-I kappa B- alpha, P-p65 expression level is obviously elevated).4.Mer TK through the signaling pathway and the negative protein to induce the negative inflammatory reaction Under the action of LTA stimulation, the activation of Akt and SOCS3 is Mer TK dependent. At the same time, the activation of Akt and SOCS3 induced by LTA can be prevented by the use of specific Mer inhibition antibody preconditioning. Moreover, PI3K/Akt pathway and SOCS3 protein inhibit the inflammatory response mediated by LTA. The activation.2.Mer TK of the anti inflammatory signaling pathway of Mer TK through the PI3K/Akt pathway and SOCS3 protein to negatively regulate the inflammatory response induced by LTA. Two.Mer TK in macrophages phagocytic Staphylococcus aureus? Research background is present. Studies have shown that many receptors expressed on the surface of macrophages are involved in the identification of apoptotic cells and bacteria. Phagocytosis, including SR-A, CD14, integrin, complement receptor and Fc receptor. In addition, the rapid phagocytosis of Mer TK expressed on the surface of macrophages is essential. Therefore, we investigate whether the Mer TK receptor is also involved in the phagocytosis of the bacteria. Objective 1. Staphylococcus aureus to stimulate RAW264.7 macrophages and to detect the phagocytic signal The expression of related protein.2. in the study of the role of Mer TK in phagocytosis of Staphylococcus aureus in RAW264.7 macrophages. Methods 1.Western Blot was used to detect the expression of associated proteins in macrophages by Staphylococcus aureus using Staphylococcus aureus at different time (20min, 40min, 60min, 120min) to stimulate RAW264.7 giant macrophages. Then, the Staphylococcus aureus was detected by Western methodology. The expression level of related protein molecules in the process of stimulating RAW264.7 macrophages.2. respectively study the effect of Mer TK on macrophage phagocytic Staphylococcus from protein molecular level and morphology. We detected the effect of Mer TK on the phagocytic protein molecules of RAW264.7 macrophages from the protein molecular level. The specific Mer inhibition antibody was used. RAW264.7 macrophage 1H, then Staphylococcus aureus was used to stimulate RAW264.7 cell 1H. First, the Western Blot method was used to detect the expression level of the phagocytic protein P-FAK and GTP-Rac1. Secondly, the phagocytic ability of RAW264.7 cells phagocytic Staphylococcus was evaluated by phagocytic test. Results 1. Staphylococcus aureus stimulates RAW264.7 cells can cause its table. The activation of RAW264.7 cells by activated Staphylococcus aureus from various receptor molecules can cause activation of a variety of receptor molecules on the surface, including the TLR2 signaling pathway (My D88, p65, JNK, ERK, p38), SR-A and Mer TK, and their activation in a time-dependent manner can induce the activation and activation of the phagocytic associated protein and the activation of the cells. At the time, Staphylococcus aureus stimulated RAW264.7 cells to increase the level of FAK phosphorylation and increase the level of GTP-Rac1 expression of Rac1 activation, and also in a time dependent manner,.3. targeting Mer TK had no significant effect on the activation of FAK and Rac1 induced by Staphylococcus aureus by Mer TK, using specific Mer inhibition antibody preprocessing RAW264.7 macrophage 1 H, then using Staphylococcus aureus to stimulate the RAW264.7 cell 1H, then we detected the effect of this specific Mer inhibitory antibody on the phagocytic signaling pathway related protein P-FAK and GTP-Rac1 from the protein molecular level. We found that this antibody has no significant effect on the P-FAK and GTP-Rac1 expression level of the Staphylococcus aureus stimulated RAW264.7 cell activation of.4.Mer TK to the giant. The ability of phagocytic phagocytosis of Staphylococcus aureus has no significant effect to further confirm the role of Mer TK in macrophage phagocytosis of Staphylococcus aureus. We assessed the ability of RAW264.7 macrophages to phagocytate Staphylococcus aureus by phagocytosis test. We found that RAW264.7 cells phagocytosis of Staphylococcus aureus after specific Mer suppression antibody preconditioning No significant changes. Conclusion 1. Staphylococcus aureus stimulated macrophages to induce phagocytic signal and Mer TK activation.2., however, Mer TK was not important for macrophage phagocytosis of Staphylococcus aureus.
【學(xué)位授予單位】：安徽醫(yī)科大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2016
【分類號】：R392

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