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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 何藴芳(Yunn-Fang Ho) | |
dc.contributor.author | Chi-Pau Hung | en |
dc.contributor.author | 洪啟堡 | zh_TW |
dc.date.accessioned | 2023-03-19T22:10:01Z | - |
dc.date.copyright | 2022-10-17 | |
dc.date.issued | 2022 | |
dc.date.submitted | 2022-09-26 | |
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dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/84386 | - |
dc.description.abstract | 研究背景 巨噬細胞在非結核性分枝桿菌(nontuberculous mycobacteria,NTM)感染中扮演重要角色,NTM可以將巨噬細胞做為蓄積庫,進而潛藏於其胞內,阻礙藥品有效作用,除非,能有足量藥品適時進入巨噬細胞內發揮作用。未活化的巨噬細胞(nave macrophage,M0)經極化作用(polarization)後,會形成兩種型態:古典活化巨噬細胞(classical activated macrophage, M1)與替代活化巨噬細胞(alternatively activated macrophage, M2)。先前U937細胞株之M1與M2分化研究顯示,會影響P-glycoprotein(P-gp)等藥物外排轉運蛋白之表現量,而mRNA或轉運蛋白表現量的差異,則會影響巨噬細胞對藥品的攝取,進而可能造成NTM感染症藥物治療效用難以預期。 Amikacin(胺羥康絲菌素)屬胺基苷類抗生素(aminoglycoside antibiotics),臨床上主要用於治療革蘭氏陰性菌與分枝桿菌所引起的感染症,特別是在臨床棘手情境之處置上,如對巨環類抗生素有抗藥性或嚴重NTM肺部感染症(NTM-pulmonary disease,NTM-PD)。在臨床治療上,即使痰液培養呈陰性,仍需接受為期一年的amikacin藥物治療,以確保不會有NTM於巨噬細胞存活並增生。於小鼠動物模式研究中,發現amikacin與P-gp抑制劑併用,得以提升細胞對於amikacin的攝取,然而在人類細胞,amikacin與P-gp間之關連性,則尚待探討。 研究目的 藉由人類血癌單核球THP-1細胞株,建立巨噬細胞分化模型,釐清P-gp與amikacin間,於人類細胞株是否存在轉運蛋白-受質關係,並進一步運用藥物調控P-gp功能,探討巨噬細胞內amikacin濃度變化。 研究方法 本研究使用THP-1細胞建立巨噬細胞分化模型,進而使用流式細胞儀、即時聚合酶連鎖反應及酵素結合免疫吸附分析法,確認細胞分化狀態。P-gp的表現量及功能檢測,則分別利用西方墨點法及螢光染劑分析法偵測。最後透過amikacin(3.25 mg/mL)與P-gp抑制劑(elacridar,10 mM ; verapamil, 10、50、100 mM)分別併用,以酵素結合免疫吸附分析法定量amikacin濃度,分析細胞內與細胞外amikacin依時序之濃度變化。 研究結果 經由細胞表面標誌、蛋白質表現量及細胞激素(cytokines)分泌情形,確認成功分化THP-1為M1或M2巨噬細胞。經西方墨點法分析,M2巨噬細胞P-gp表現量(415.4 ± 6.3%)顯著高於M0(100.0 ± 0%)(p < 0.0001)與M1(147.2 ± 4.0%)(p < 0.0001)巨噬細胞。在P-gp表現量最高的M2巨噬細胞中,觀察到胞內amikacin濃度最低,顯示胞內amikacin濃度與P-gp表現量呈現負相關性。在amikacin與P-gp抑製劑併用實驗中,給予相同濃度elacridar(10 mM),顯著提升M2之胞內amikacin濃度;在給予不等濃度verapamil(10、50、100 mM)的組別中,亦觀察到相同的趨勢。 結論 THP-1分化成之M1與M2巨噬細胞膜上,呈現藥物外排轉運蛋白P-gp之表現,且M2之表現量高於M1,而P-gp表現量或功能和細胞內amikacin濃度具負相關。透過併用amikacin與P-gp抑製劑,將得以調控細胞內藥品濃度,有助解決抗藥性難題。 | zh_TW |
dc.description.abstract | Background Macrophages play an important role in the infection of nontuberculous mycobacteria (NTM). NTM can employ macrophages as a reservoir to escape drug effects by hiding within the reservoir, unless sufficient drug levels provided. Nave macrophages (M0) can undergo polarization toward either classically activated macrophages (M1) or alternatively activated macrophages (M2). Previous study demonstrated that the M1 or M2 differentiation of the U937 cell line altered the expressions of P-glycoprotein (P-gp) and certain drug efflux transporters. The altered expressions in transporter mRNA or proteins would have direct impact on drug uptake by macrophages, resulting in unpredictable drug efficacy in the treatment of NTM infection. Amikacin is an aminoglycoside antibiotic that is used for the treatment of severe infections caused by Gram-negative bacteria and mycobacteria, especially the macrolide-resistant NTM pulmonary disease (NTM-PD). In clinical, amikacin treatment for NTM-PD should continue for a minimum of 12 months after culture conversion to ensure that no NTM can survive and proliferate in macrophages. It was found that the combination of amikacin and P-gp inhibitors can improve the cellular uptake of amikacin in mice animal model. However, the relationship between amikacin and P-gp in human cells remains to be explored. Objectives We aimed to establish a macrophage differentiation model using human monocytic leukemia cell line THP-1 to clarify whether there is a transporter–substrate relationship between P-gp and amikacin in human cell lines, and to use P-gp modulators to examine possible changes in amikacin concentrations inside macrophages. Methods THP-1 cells were used in this study to establish a macrophage differentiation model. Flow cytometry, qPCR, and enzyme-linked immunosorbent assay were used to confirm M1/M2 polarity of the established model. The expression and function of P-gp were assessed using Western blotting, confocal imaging, and fluorescent dye assays. Modulation of intracellular and extracellular amikacin concentrations by concurrent administration of amikacin (3.25 mg/mL) and P-gp inhibitors (elacridar:10 mM; Verapamil: 10, 50, and 100 mM) were investigated. Amikacin concentrations were determined by enzyme-linked immunosorbent assay. Results The differentiation of THP-1 into M1 or M2 macrophages was confirmed based on positive expressions of respective cell surface markers and cytokine secretions. Western blot analysis revealed that the expression of P-gp in M2 macrophages (415.4 ± 6.3%) was significantly higher than those in M0 (100.0 ± 0%; p < 0.0001) and M1 (147.2 ± 4.0%; p < 0.0001) macrophages. The intracellular amikacin level was negatively correlated with the expression of P-gp, namely the lowest intracellular concentrations of amikacin were observed in M2 macrophages with the highest expression of P-gp. Furthermore, intracellular amikacin concentrations of M2 macrophages were noticeably enhanced upon elacridar co-administration. Cells co-treated with varying concentrations of verapamil also exhibited similar trend. Conclusion Differential expression of drug efflux transporter P-gp was observed in the established M1 and M2 macrophage model. The M2 macrophage had higher P-gp expression levels than M1 and lower intracellular amikacin levles. Furthermore, concurrent administration of amikacin and P-gp inhibitors led to increased intracellular amikacin levels. To tackle the challenge of drug resistance, the study supports the emerging concept of attaining efficacious drug levels in targeted cells by co-administration of modulators of drug transporters. | en |
dc.description.provenance | Made available in DSpace on 2023-03-19T22:10:01Z (GMT). No. of bitstreams: 1 U0001-2309202216453600.pdf: 2690553 bytes, checksum: 4b5e22ff699d3793f2c8ac485827ea02 (MD5) Previous issue date: 2022 | en |
dc.description.tableofcontents | 致謝 i 摘要 iii Abstract v Table of Contents viii List of Figure xi List of Table xii List of Abbreviation xiii Chapter 1 Introduction 1 1.1 Brief concept of Drug Interaction 1 1.2 Macrophages 2 1.2.1 M1 macrophages 2 1.2.2 Markers of M1 macrophages 3 1.2.3 M2 macrophages 5 1.2.4 Markers of M2 macrophages 6 1.2.5 Methods on the studies of macrophages 7 1.2.6 M1 and M2 macrophages antimicrobial activity 9 1.2.7 Antibiotics resistance issue in macrophages 10 1.3 P-glycoprotein 14 1.3.1 Distributions of P-gp 14 1.3.2 P-gp affects drug therapeutic levels 14 1.3.3 Methods on the studies of P-gp 16 1.3.4 P-gp inhibitors 16 1.4 Nontuberculous mycobacteria 18 1.5 Amikacin 20 1.5.1 Therapeutic target range 20 1.5.2 Pharmcokinetics paramrters 21 1.5.3 Amikacin associated transporters 21 1.5.4 Methods of analysis amikacin concentration 21 1.6 THP-1 cell line 24 Chapter 2 Objectives 27 Chapter 3 Materials and Methods 29 3.1 Cell culture 29 3.2 Macrophage differentiation and polarization 29 3.3 RNA extraction 29 3.3.1 Extraction RNA from cells 29 3.3.2 Quality control 30 3.4 RT-qPCR 30 3.4.1 Reverse transcription 30 3.4.2 Real time- quantitative polymerase chain reaction 31 3.5 Flow cytometry and antibodies 32 3.6 Quantification of IL-6, TNF-α, IL-10, and CCL-18 in the culture medium 32 3.7 Western bolt analysis 35 3.7.1 Extraction of cell protein 35 3.7.2 Quantification of protein concentration 35 3.7.3 Western blot 36 3.8 R123 efflux assay 38 3.9 Confocal microscopy 39 3.10 Quantification of intracellular amikacin concentrations 40 3.10.1 Sample collection 40 3.10.2 Amikacin ELISA analysis 40 3.11 Statistical analysis 41 Chapter 4 Results 43 4.1 Characterization of M1 and M2 macrophages 43 4.2 Differential expression of P-glycoprotein in M1 and M2 macrophages 44 4.3 Relative P-glycoprotein activities in polarized macrophages 45 4.4 Camprasion of intracellular amikacin levels in macrophages 45 4.5 Efects of verapamil in intracellular amikacin levels in polarized macrophages 46 Chapter 5 Discussion 55 Chapter 6 Conclusion 61 References 62 Appendix 77 List of Figure Figure 1-1 Classification of SLC ABC-carriers in the plasma membrane 25 Figure 1-2 Overview of M1 and M2 macrophages 25 Figure 1-3 Molecular structures of verapamil and elacridar 26 Figure 1-4 Molecular structure of amikacin 26 Figure 2-1 Study hypotheses and objectives 28 Figure 3-1 Experimental study design 42 Figure 4-1 Characterization of M1 and M2 macrophages 48 Figure 4-2 M1 and M2 markers of polarized macrophages 49 Figure 4-3 Pro-inflammatory and anti-inflammatory cytokines secretion in culture medium 50 Figure 4-4 The expression of P-gp in polarized macrophages 51 Figure 4-5 Relative P-glycoprotein activities in polarized macrophages 52 Figure 4-6 Intracellular concentrations of amikacin in polarized macrophages 53 Figure 4-7 Effects of verapamil on intracellular amikacin levels in polarized macrophages 54 Figure A1 Effects of amikacin on THP-1 cell viabilities 78 Figure A2 Extracellular concentrations of amikacin in polarized macrophages 79 Figure A3 Effects of accutase on the expression of M2 macrophages surface markers 80 List of Table Table A1. The list of primers used for RT-qPCR 77 Table A2. The list of antibodies used for flow cytometry 77 | |
dc.language.iso | en | |
dc.title | 以THP-1巨噬細胞研究P-glycoprotein表現量之調控對於細胞內amikacin濃度之影響 | zh_TW |
dc.title | The effect of modulation of P-glycoprotein expressions on the intracellular amikacin levels in THP-1 macrophages | en |
dc.type | Thesis | |
dc.date.schoolyear | 110-2 | |
dc.description.degree | 碩士 | |
dc.contributor.oralexamcommittee | 林君榮(Chun-Jung Lin),黃彥銘(Yen-Ming Huang),王振源(Jann-Yuan Wang) | |
dc.subject.keyword | 巨噬細胞,P-glycoprotein,THP-1細胞,胺羥康絲菌素,NTM感染, | zh_TW |
dc.subject.keyword | Macrophages,P-glycoprotein,THP-1 cells,Amikacin,NTM infections, | en |
dc.relation.page | 80 | |
dc.identifier.doi | 10.6342/NTU202203934 | |
dc.rights.note | 同意授權(限校園內公開) | |
dc.date.accepted | 2022-09-27 | |
dc.contributor.author-college | 醫學院 | zh_TW |
dc.contributor.author-dept | 藥學研究所 | zh_TW |
dc.date.embargo-lift | 2022-10-17 | - |
顯示於系所單位: | 藥學系 |
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