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<p><i>Klebsiella pneumoniae</i> is an important pathogen, especially hypervirulent and multidrug-resistant <i>K. pneumoniae</i>, which are increasingly becoming a serious threat to global public health. Bacteriophages and their depolymerases are promising therapeutic alternatives to antibiotics as they are effective against hypervirulent and multidrug-resistant <i>K. pneumoniae</i> infections. In this study, we identified the novel depolymerase K57-Dpo8 from <i>K. pneumoniae</i> phage P5054. K57-Dpo8 exhibited specific depolymerase activity against K57-type capsular polysaccharide, increasing the susceptibility of K57-type <i>K. pneumoniae</i> strains to serum killing, macrophage phagocytosis, and improving survival rates in a murine infection model. K57-Dpo8 could inhibit biofilm formation and degrade formed biofilms. Our results provide evidence that K57-Dpo8 is not only effective for capsular typing of K57-type <i>K. pneumoniae</i> but also represents a promising alternative therapeutic strategy for treating K57-type <i>K. pneumoniae</i> infections.</p>

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A novel depolymerase encoded by phage P5054 specifically degrades the K57-type capsular polysaccharide of Klebsiella pneumoniae

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月16日

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  • Heyuan Lun,
  • Juanjuan Wang,
  • Huagen Chen,
  • Heng Li,
  • Ruijing Ma,
  • Yuqing Pan,
  • Tingting Qu,
  • Aixi Wang,
  • Kai He,
  • Jingran Yu,
  • Ping He

摘要

Klebsiella pneumoniae is an important pathogen, especially hypervirulent and multidrug-resistant K. pneumoniae, which are increasingly becoming a serious threat to global public health. Bacteriophages and their depolymerases are promising therapeutic alternatives to antibiotics as they are effective against hypervirulent and multidrug-resistant K. pneumoniae infections. In this study, we identified the novel depolymerase K57-Dpo8 from K. pneumoniae phage P5054. K57-Dpo8 exhibited specific depolymerase activity against K57-type capsular polysaccharide, increasing the susceptibility of K57-type K. pneumoniae strains to serum killing, macrophage phagocytosis, and improving survival rates in a murine infection model. K57-Dpo8 could inhibit biofilm formation and degrade formed biofilms. Our results provide evidence that K57-Dpo8 is not only effective for capsular typing of K57-type K. pneumoniae but also represents a promising alternative therapeutic strategy for treating K57-type K. pneumoniae infections.