Three Capsular Polysaccharide Synthesis-Related Glucosyltransferases, GT-1, GT-2 and WcaJ, Are Associated With Virulence and Phage Sensitivity of Klebsiella pneumoniae
Klebsiella pneumoniae (K. pneumoniae) spp. are important nosocomial and community-acquired opportunistic pathogens, which cause various infections. We observed that K. pneumoniae strain K7 abruptly mutates to rough-type phage-resistant phenotype upon treatment with phage GH-K3. In the present study, the rough-type phage-resistant mutant named K7RR showed much lower virulence than K7. Liquid chromatography-tandem mass spectrometry (LC-MS-MS) analysis indicated that WcaJ and two undefined glycosyltransferases (GTs)- named GT-1, GT-2- were found to be down-regulated drastically in K7RR as compared to K7 strain. GT-1, GT-2, and wcaJ are all located in the gene cluster of capsular polysaccharide (CPS). Upon deletion, even of single component, of GT-1, GT-2, and wcaJ resulted clearly in significant decline of CPS synthesis with concomitant development of GH-K3 resistance and decline of virulence of K. pneumoniae, indicating that all these three GTs are more likely involved in maintenance of phage sensitivity and bacterial virulence. Additionally, K7RR and GT-deficient strains were found sensitive to endocytosis of macrophages. Mitogen-activated protein kinase (MAPK) signaling pathway of macrophages was significantly activated by K7RR and GT-deficient strains comparing with that of K7. Interestingly, in the presence of macromolecular CPS residues (>250 KD), K7(ΔGT-1) and K7(ΔwcaJ) could still be bounded by GH-K3, though with a modest adsorption efficiency, and showed minor virulence, suggesting that the CPS residues accumulated upon deletion of GT-1 or wcaJ did retain phage binding sites as well maintain mild virulence. In brief, our study defines, for the first time, the potential roles of GT-1, GT-2, and WcaJ in K. pneumoniae in bacterial virulence and generation of rough-type mutation under the pressure of bacteriophage.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2019 |
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Erschienen: |
2019 |
Enthalten in: |
Zur Gesamtaufnahme - volume:10 |
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Enthalten in: |
Frontiers in microbiology - 10(2019) vom: 01., Seite 1189 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Cai, Ruopeng [VerfasserIn] |
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Links: |
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Themen: |
Glucosyltransferase (GT) |
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Anmerkungen: |
Date Revised 30.09.2020 published: Electronic-eCollection Citation Status PubMed-not-MEDLINE |
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doi: |
10.3389/fmicb.2019.01189 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM298083892 |
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520 | |a Klebsiella pneumoniae (K. pneumoniae) spp. are important nosocomial and community-acquired opportunistic pathogens, which cause various infections. We observed that K. pneumoniae strain K7 abruptly mutates to rough-type phage-resistant phenotype upon treatment with phage GH-K3. In the present study, the rough-type phage-resistant mutant named K7RR showed much lower virulence than K7. Liquid chromatography-tandem mass spectrometry (LC-MS-MS) analysis indicated that WcaJ and two undefined glycosyltransferases (GTs)- named GT-1, GT-2- were found to be down-regulated drastically in K7RR as compared to K7 strain. GT-1, GT-2, and wcaJ are all located in the gene cluster of capsular polysaccharide (CPS). Upon deletion, even of single component, of GT-1, GT-2, and wcaJ resulted clearly in significant decline of CPS synthesis with concomitant development of GH-K3 resistance and decline of virulence of K. pneumoniae, indicating that all these three GTs are more likely involved in maintenance of phage sensitivity and bacterial virulence. Additionally, K7RR and GT-deficient strains were found sensitive to endocytosis of macrophages. Mitogen-activated protein kinase (MAPK) signaling pathway of macrophages was significantly activated by K7RR and GT-deficient strains comparing with that of K7. Interestingly, in the presence of macromolecular CPS residues (>250 KD), K7(ΔGT-1) and K7(ΔwcaJ) could still be bounded by GH-K3, though with a modest adsorption efficiency, and showed minor virulence, suggesting that the CPS residues accumulated upon deletion of GT-1 or wcaJ did retain phage binding sites as well maintain mild virulence. In brief, our study defines, for the first time, the potential roles of GT-1, GT-2, and WcaJ in K. pneumoniae in bacterial virulence and generation of rough-type mutation under the pressure of bacteriophage | ||
650 | 4 | |a Journal Article | |
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700 | 1 | |a Wang, Gang |e verfasserin |4 aut | |
700 | 1 | |a Le, Shuai |e verfasserin |4 aut | |
700 | 1 | |a Wu, Mei |e verfasserin |4 aut | |
700 | 1 | |a Cheng, Mengjun |e verfasserin |4 aut | |
700 | 1 | |a Guo, Zhimin |e verfasserin |4 aut | |
700 | 1 | |a Ji, Yalu |e verfasserin |4 aut | |
700 | 1 | |a Xi, Hengyu |e verfasserin |4 aut | |
700 | 1 | |a Zhao, Caijun |e verfasserin |4 aut | |
700 | 1 | |a Wang, Xinwu |e verfasserin |4 aut | |
700 | 1 | |a Xue, Yibing |e verfasserin |4 aut | |
700 | 1 | |a Wang, Zijing |e verfasserin |4 aut | |
700 | 1 | |a Zhang, Hao |e verfasserin |4 aut | |
700 | 1 | |a Fu, Yunhe |e verfasserin |4 aut | |
700 | 1 | |a Sun, Changjiang |e verfasserin |4 aut | |
700 | 1 | |a Feng, Xin |e verfasserin |4 aut | |
700 | 1 | |a Lei, Liancheng |e verfasserin |4 aut | |
700 | 1 | |a Yang, Yongjun |e verfasserin |4 aut | |
700 | 1 | |a Ur Rahman, Sadeeq |e verfasserin |4 aut | |
700 | 1 | |a Liu, Xiaoyun |e verfasserin |4 aut | |
700 | 1 | |a Han, Wenyu |e verfasserin |4 aut | |
700 | 1 | |a Gu, Jingmin |e verfasserin |4 aut | |
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