Anti-PD-1 Therapy Alleviates Klebsiella pneumoniae-Induced Liver Abscess by Effectively Activating Kupffer Cells.

Authors

Huaxiu You, Minlie Liang, Houxiong Lin, Ying Liu, Xian Huang, Yuanzhong Gong

Published in

Journal of microbiology and biotechnology. Volume 36. Pages e2602040. Oct 19, 2026. Epub Oct 19, 2026.

Abstract

Klebsiella pneumoniae-induced liver abscess (KPLA) is the leading cause of pyogenic liver abscess (LA) worldwide. Hepatic Kupffer cells exert protective effects during KPLA progression; thus, elucidating their protective mechanisms and developing novel therapeutic strategies are imperative. A murine KPLA model was established. Hematoxylineosin (HE) staining and tissue bacterial load were analyzed to verify successful K. pneumoniae infection. RT-qPCR, Western blot (WB), and flow cytometry were employed to quantify PD-1 expression in Kupffer cells. PD-1-knockdown Kupffer-cell transfection systems and PD-1-antibody treatment groups were established. Bacterial counts (CFU) and ELISA plus flow cytometry for inflammatory cytokines were used to evaluate the relationship between PD-1 expression and Kupffer-cell bacterial clearance. Finally, the KPLA mouse model was treated with PD-1 antibody to validate the role of PD-1 in LA. In the KPLA mouse model, gross abscess formation was observed, and HE staining revealed disorganized hepatic architecture. PD-1 expression in Kupffer cells was markedly up-regulated, and the proportion of PD-1-positive Kupffer cells increased significantly. In vitro, both PD-1 knockdown and PD-1-antibody treatment enhanced Kupffer-cell bacterial clearance, accompanied by elevated TNF-α, IL-6, and IL-12 levels. In vivo, the PD-1 antibody effectively treated KPLA. KPLA up-regulates PD-1 expression in Kupffer cells, thereby impairing bacterial clearance. Our findings preliminarily indicate that the anti-PD-1 antibody may have application potential in the prevention or early intervention of KPLA.

PMID:
42894963
Bibliographic data and abstract were imported from PubMed on 19 Oct 2026.

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