Autophagy, cell death, and cytokines in K. pneumoniae infection: therapeutic perspectives

Emerg Microbes Infect. 2023 Dec;12(1):2140607. doi: 10.1080/22221751.2022.2140607.

Abstract

Klebsiella pneumoniae is a notorious nosocomial pathogen causing a wide range of infections. The increasing trend of antimicrobial resistance obtained by the species immensely highly challenges the clinical treatment, representing a large threat to the global health care network. In particular, the recent convergence of multidrug resistance and hypervirulence in K. pneumoniae further worsens clinical outcomes, resulting in high mortality. Developments of new therapeutics become urgent, and immunotherapy based on antagonizing the anti-immune strategies of pathogens is a promising strategy, which requires the understanding of immune evasion mechanism in the context of the host-pathogen interactions. However, the underlying mechanisms employed by K. pneumoniae to counteract host immune responses, especially autophagy and cell death, have not been systematically reviewed and discussed yet. This review aims to summarize the tremendous progress that has been made to illuminate the landscape of cell signalling triggered by K. pneumoniae infection, especially in aspects of manipulating autophagy, cell death, and cytokine production.

Keywords: Klebsiella pneumoniae; apoptosis; autophagy; cytokines; necrosis; pyroptosis.

Publication types

  • Review

MeSH terms

  • Anti-Bacterial Agents / therapeutic use
  • Autophagy
  • Cell Death
  • Cytokines
  • Humans
  • Klebsiella Infections* / drug therapy
  • Klebsiella pneumoniae*

Substances

  • Cytokines
  • Anti-Bacterial Agents

Grants and funding

This work was supported by the National Key R&D Program of China (grant numbers 2021YFC2300300 and 2022YFE0103200), National Natural Science Foundation of China (grant numbers 82002105, 82172330 and 81902030), Shenzhen Basic Research Key Project (grant number JCYJ20200109144220704) and Shenzhen Basic Research Project (grant number JCYJ20190807144409307).