江倪全

江倪全

江倪全 (Chuan Chiang-Ni)

職稱:教授

研究室名稱:細菌致病機轉實驗室

最高學歷:Ph.D.

學校/國家: 成功大學/中華民國 (台灣)

分機號碼:03-2118800 ext.3712

電子郵件帳號: entchuan@gap.cgu.edu.tw

個人網頁網址: 

研究室現有:

博士後研究員 0 人

博士班研究生 1 人

碩士班研究生 3 人

專任研究助理 1 人

大學部專題生 2 人

研究方向及研究室特色

    化膿性鏈球菌 (Streptococcus pyogenes) 是革蘭氏陽性的人類致病菌。常造成細菌性咽喉炎、猩紅熱、以及傷口感染。傷口感染沒有及早就醫,可能會進一步會形成蜂窩性組織炎或是壞死性肌膜炎,由於這些疾病會造成嚴重的肌肉組織壞死,因此這隻細菌有另一個惡名昭彰的名字:噬肉菌。

    觀測化膿性鏈球菌所造成的感染發現一個非常特別的現像,就是在造成嚴重的感染後,原本的化膿性鏈球菌在動物體內會變成兩種族群,其中一種族群和一開始造成病人感染的細菌有相同的表現型;然而另一種族群則是呈現莢膜大量表現的型態。由於莢膜是細菌造成感染的毒力因子之一,因此,此具有莢膜大量表現的化膿性鏈球菌,和原本的菌株相較,會對實驗動物造成更嚴重的感染疾病。目前的研究已知,這些莢膜大量表現的化膿性鏈球菌菌株,是因為細菌體中其中一個控制莢膜表現的調控因子發生了突變。在感染的過程,這些發生基因突變的細菌,比沒有發生突變的細菌有更厚的莢膜,所以具有更強的毒性及更好抵抗白血球吞噬的能力。因此,在宿主的體內,原先具有突變的菌株可能只是一個很小的族群,然而,因為白血球等免疫系統的壓力,這個突變的族群就有可能變成主要的族群,之後並更進一步的造成嚴重的感染疾病。

    根據物競天擇 "適者生存,不適者淘汰" 的法則,我們在臨床上應該要看到大多數病人身上所分離出來的化膿性鏈球菌是要有基因突變且具有厚莢膜的表現型。然而,與這個推論相反,大部份所分離到的化膿性鏈球菌菌株,卻都沒有基因突變,且不是有厚莢膜的表現型。為什麼?這些突變的菌株不是毒性比較強嗎?最可能的解釋是,具有基因突變而有厚莢膜表現型的化膿性鏈球菌,可能只有在一個非常特定的環境下有選擇性上的優勢,而在一般的環境,或是在一些比較輕微的感染情況下,其實無法與沒有基因突變的菌株競爭。所以,到底是什麼環境壓力可以選擇出這些毒性較強的菌株?回答這個問題可能可以進一步提供我們發展預防嚴重化膿性鏈球菌感染的策略。

目前實驗室的研究主軸包括:

  • 研究此兩種不同表現型的菌株在不同環境壓力下的適應力。
  • 研究有基因突變且具有厚莢膜表現型的菌株為何具有較強的毒性。
  • 研究相關基因之轉錄調控及訊號傳遞機制。

近五年發表論文

Publications: 2020-2016 (*: Corresponding author)

  • Hsieh CL, Hsieh SY, Huang HM, Lu SL, Omori H, Zheng PX, Ho YN, Cheng YL, Lin YS, Chiang-Ni C, Tsai PJ, Wang SY, Liu CC, Noda T, Wu JJ*. 2020. Nicotinamide increases intracellular NAD(+) Content to enhance autophagy-mediated group A streptococcal clearance in endothelial cells. Front Microbiol 11:117. https://doi.org/10.3389/fmicb.2020.00117
  • Chiang-Ni C*, Chiou HJ, Tseng HC, Hsu CY, Chiu CH. 2020. RocA regulates phosphatase activity of virulence sensor CovS of group A Streptococcus in growth phase- and pH-dependent manners. mSphere 5:e00361-00320. https://doi.org/10.1128/msphere.00361-20
  • Chen YW, Huang MZ, Chen CL, Kuo CY, Yang CY, Chiang-Ni C, Chen YM, Hsieh CM, Wu HY, Kuo ML, Chiu CH, Lai CH*. 2020. PM2.5 impairs macrophage functions to exacerbate pneumococcus-induced pulmonary pathogenesis. Part Fibre Toxicol 17:37. https://doi.org/10.1186/s12989-020-00362-2
  • Hou TY, Chiang-Ni C, Teng SH*. 2019. Current status of MALDI-TOF mass spectrometry in clinical microbiology. J Food Drug Anal 27:404-414. https://doi.org/10.1016/j.jfda.2019.01.001
  • Chiang-Ni C*, Tseng HC, Shi YA, Chiu CH. 2019. Effect of phosphatase activity of the control of virulence sensor (CovS) on clindamycin-mediated streptolysin O production in group A Streptococcus. Infect Immun 87:e00583-00519. https://doi.org/10.1128/IAI.00583-19
  • Chiang-Ni C*, Kao CY, Hsu CY, Chiu CH. 2019. Phosphorylation at the D53 but not T65 residue of CovR determines the repression of rgg and speB transcription in emm1- and emm49-type group A streptococci. J Bacteriol 201:e00681-00618. https://doi.org/10.1128/JB.00681-18
  • Chen MF, Chang CH, Chiang-Ni C, Hsieh PH, Shih HN, Ueng SWN, Chang Y*. 2019. Rapid analysis of bacterial composition in prosthetic joint infection by 16S rRNA metagenomic sequencing. Bone Joint Res 8:367-377. https://doi.org/10.1302/2046-3758.88.BJR-2019-0003.R2
  • Hsieh CL, Huang HM, Hsieh SY, Zheng PX, Lin YS, Chiang-Ni C, Tsai PJ, Wang SY, Liu CC, Wu JJ*. 2018. NAD-glycohydrolase depletes intracellular NAD(+) and inhibits acidification of autophagosomes to enhance multiplication of group A Streptococcus in endothelial cells. Front Microbiol 9:1733. https://doi.org/10.3389/fmicb.2018.01733
  • Chiang-Ni C*, Shi YA, Lai CH, Chiu CH. 2018. Cytotoxicity and survival fitness of Invasive covS mutant of group A Streptococcus in phagocytic cells. Front Microbiol 9:2592. https://doi.org/10.3389/fmicb.2018.02592
  • Zheng PX, Chan YC, Chiou CS, Hsieh CL, Chiang-Ni C, Wu JJ*. 2017. Highly prevalent emmSTG840.0 and emmSTC839.0 types of erythromycin non-susceptible group G Streptococcus isolated from bacteremia in southern Taiwan. J Microbiol Immunol Infect 50:831-838. https://doi.org/10.1016/j.jmii.2016.12.010
  • Lin HJ, Liu HH, Lin CD, Kao MC, Chen YA, Chiang-Ni C, Jiang ZP, Huang MZ, Lin CJ, Lo UG, Lin LC, Lai CK, Lin H, Hsieh JT, Chiu CH, Lai CH*. 2017. Cytolethal distending toxin enhances radiosensitivity in prostate cancer cells by regulating autophagy. Front Cell Infect Microbiol 7:223. https://doi.org/10.3389/fcimb.2017.00223
  • Hou JN, Chen TH, Chiang YH, Peng JY, Yang TH, Cheng CC, Sofiyatun E, Chiu CH, Chiang-Ni C, Chen WJ. 2017. PERK signal-modulated protein translation promotes the survivability of Dengue 2 virus-infected mosquito cells and extends viral replication. Viruses 9. https://doi.org/10.3390/v9090262
  • Chiang-Ni C*, Tseng HC, Hung CH, Chiu CH. 2017. Acidic stress enhances CovR/S-dependent gene repression through activation of the covR/S promoter in emm1-type group A Streptococcus. Int J Med Microbiol 307:329-339. https://doi.org/10.1016/j.ijmm.2017.06.002
  • Lai CK, Chen YA, Lin CJ, Lin HJ, Kao MC, Huang MZ, Lin YH, Chiang-Ni C, Chen CJ, Lo UG, Lin LC, Lin H, Hsieh JT, Lai CH*. 2016. Molecular mechanisms and potential clinical applications of Campylobacter jejuni cytolethal distending toxin. Front Cell Infect Microbiol 6:9. https://doi.org/10.3389/fcimb.2016.00009
  • Lai CH*, Huang JC, Chiang-Ni C, Li JP, Wu LT, Wu HS, Sun YC, Lin ML, Lee JF, Lin HJ. 2016. Mixed infections of Helicobacter pylori isolated from patients with gastrointestinal diseases in Taiwan. Gastroenterol Res Pract 2016:7521913. https://doi.org/10.1155/2016/7521913
  • Chiang-Ni C, Zheng PX, Wang SY, Tsai PJ, Chuang WJ, Lin YS, Liu CC, Wu JJ*. 2016. Epidemiology analysis of Streptococcus pyogenes in a hospital in Southern Taiwan by use of the updated emm cluster typing system. J Clin Microbiol 54:157-162. https://doi.org/10.1128/JCM.02089-15
  • Chiang-Ni C*, Nian SY, Wu JJ, Chen CJ. 2016. Oxygen-dependent phenotypic variation in group A streptococcus. J Microbiol Immunol Infect 49:837-842. https://doi.org/10.1016/j.jmii.2014.11.010
  • Chiang-Ni C*, Chu TP, Wu JJ, Chiu CH. 2016. Repression of Rgg but not upregulation of LacD.1 in emm1-type covS mutant mediates the SpeB repression in group A Streptococcus. Front Microbiol 7:1935. https://doi.org/10.3389/fmicb.2016.01935