Authors
Ju Yeong Lee, Hui-Jung Jung, Anwesha Ash, Seunghyeon Jeon, Miri Hyun, Ji Yeon Lee, Sang-Hee Lee, Hyuk Nam Kwon, Won-Ki Baek, Jichan Jang, Hyun Ah Kim, Jin Kyung Kim
Published in
Journal of microbiology (Seoul, Korea). Volume 64. Issue 8. Pages e2605001. Epub Aug 31, 2026.
Abstract
Hypervirulent Klebsiella pneumoniae (hvKp) is an emerging pathogen that causes severe community-acquired infections; however, the immune mechanisms controlling intracellular hvKp have yet to be clearly defined. In this study, we investigated the therapeutic potential of berberine against hvKp infection and elucidated the underlying molecular mechanisms using macrophage cell models and in vivo zebrafish models. Berberine significantly reduced intracellular hvKp survival in macrophages and improved survival in hvKp-infected zebrafish. Berberine markedly attenuated proinflammatory cytokine production and inhibited the c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) signaling pathways. Notably, we found that hvKp exploited host lipid droplets (LD) biosynthesis to support its intracellular survival, and berberine effectively suppressed LD accumulation. Mechanistically, berberine promoted the nuclear translocation of transcription factor EB (TFEB), thereby enhancing lipolysis. Although berberine upregulated autophagy-related gene expression during hvKp infection, it did not induce lipophagy, the selective autophagic degradation of LD. Collectively, these findings indicate that berberine has potential as a therapeutic agent against hvKp infection by modulating host lipid metabolism to restrict bacterial intracellular survival.
PMID:
42687642
Bibliographic data and abstract were imported from PubMed on 03 Sep 2026.
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