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Review

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

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Article: 2140607 | Received 03 Jul 2022, Accepted 21 Oct 2022, Published online: 18 Dec 2022
 

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.

Acknowledgements

Sha Wei and Kai Zhou prepared the manuscript. Tingting Xu helped writing the manuscript. Kai Zhou designed the study. Kai Zhou and Yuxin Chen critically edited the manuscript. All authors had full access to the manuscript and results and accept responsibility of the submission for publication.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

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).