HdeB、HdeB1、HdeD蛋白質參與克雷白氏肺炎桿菌CG43抗酸反應的探討

曾品瑄

doi:10.6842/NCTU.2011.00802

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HdeB、HdeB1、HdeD蛋白質參與克雷白氏肺炎桿菌CG43抗酸反應的探討

Study of the involvement of HdeB, HdeB1, HdeD in the acid stress response of Klebsiella pneumoniae CG43

曾品瑄 , Masters　　Advisor：彭慧玲;Hwei-Ling Peng　　

繁體中文 DOI： 10.6842/NCTU.2011.00802

抗酸；克雷白氏肺炎桿菌； HdeB ； Klebsiella pneumoniae CG43 ； acid stress response

Abstract │ Reference (74) │ Times Cited (3) │ Altmetrics

Abstract 〈TOP〉

Parallel Abstract 〈TOP〉

K. pneumoniae which is a gram-negative, opportunistic pathogen often causes diseases in hospitals including pneumonia, suppurative infection, urinary tract infections and septicemia. Before reaching the intestinal tract, they need to pass through the stomach an extremely acidic environment. How to survive this deadly acidic condition is an important issue for the bacteria to establish an infection. There are 5 acid resistance (AR) systems and an acid fitness island (AFI) containing 12 protein-encoding genes reported in Escherichia coli. Using bioinformatics tool, we have found an AFI-like DNA region which contains hdeB, hdeB1 and hdeD in the partially sequenced K. pneumoniae CG43 genome. E. coli HdeA and HdeB, activated by acidic stress, have been shown to function as chaperone in the periplasmic space to protect the proteins from damage. Here we study if HdeB, HdeB1 and HdeD play protective roles in K. pneumoniae CG43 resistance to acid stress, and HdeB and HdeB1 also act as chaperone to prevent the protein from damages. The two-component system (2CS) regulators RcsB and KvhA have been previously reported to positively regulate the promoter activity of hdeDB and hdeB1 under static-cultured condition. While under shaking-cultured condition, besides the regulation of RcsB and KvhA, the hdeDB and hdeB1 promoter activity were found to be also positively affected by the 2CS regulator PhoP and iron uptake repressor Fur. By contrast, the promoter activity of hdeDB slightly increased in the rpoS mutant. Using LacZ reporter system, we have observed that the promoter activity of hdeDB and hdeB1 in mild acid condition (pH 4.4) were slightly higher than in pH 7.0 condition. We have found that deletion of hdeB, hdeB1 or hdeD from the genome reduced the bacterial survival under acid treatments. Among them, the hdeB1 deletion mutant appeared to most sensitive to the acid-induced damages. Finally, the recombinant HdeB appeared to be able to protect ADH from the damage by the extreme acid treatment suggesting HdeB is a chaperone.

Reference ( 74 ) 〈TOP〉

1. 林志桓. 2009. Role of RcsB in acid-resistance in Klebsiella pneumoniae CG43. 國立交通大學, 生物科技學系, 碩士論文
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4. Keynan, Yoav, and Ethan Rubinstein. 2007. The changing face of Klebsiella pneumoniae infections in the community. International Journal of Antimicrobial Agents 30(5):385-389
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5. Fang, F. C., N. Sandler, and S. J. Libby. 2005. Liver Abscess Caused by magA+ Klebsiella pneumoniae in North America. Journal of Clinical Microbiology 43(2):991-992.
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6. Lederman, Edith R., and Nancy F. Crum. 2005. Pyogenic Liver Abscess with a Focus on Klebsiella pneumoniae as a Primary Pathogen: An Emerging Disease with Unique Clinical Characteristics. Am J Gastroenterol 100(2):322-331.
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7. Hyle, Emily P., et al. 2005. Risk Factors for Increasing Multidrug Resistance among Extended-Spectrum β-Lactamase-Producing Escherichia coli and Klebsiella Species. Clinical Infectious Diseases 40(9):1317-1324.
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Times Cited (3) 〈TOP〉

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