Anti-PD-1 Therapy Alleviates Klebsiella pneumoniae-Induced Liver Abscess by Effectively Activating Kupffer Cells.
- 1Department of Infectious Diseases, Nanping First Hospital Affiliated to Fujian Medical University, Nanping, Fujian, P. R. China.
- 2Department of Geriatric Medicine, Nanping First Hospital Affiliated to Fujian Medical University, Nanping, Fujian, P. R. China.
- 3Department of Infectious Diseases, Ningde Municipal Hospital of Fujian Province, Ningde, Fujian, P. R. China.
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.
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BibTeX
@article{you2026antipd1,
title = {{Anti-PD-1 Therapy Alleviates Klebsiella pneumoniae-Induced Liver Abscess by Effectively Activating Kupffer Cells.}},
author = {Huaxiu You and Minlie Liang and Houxiong Lin and Ying Liu and Xian Huang and Yuanzhong Gong},
journal = {Journal of microbiology and biotechnology},
year = {2026},
month = oct,
doi = {10.4014/jmb.2602.02040},
url = {https://europepmc.org/article/MED/42894963},
note = {CC BY},
}
RIS
TY - JOUR
TI - Anti-PD-1 Therapy Alleviates Klebsiella pneumoniae-Induced Liver Abscess by Effectively Activating Kupffer Cells.
AU - Huaxiu You
AU - Minlie Liang
AU - Houxiong Lin
AU - Ying Liu
AU - Xian Huang
AU - Yuanzhong Gong
PY - 2026
DA - 2026/10/19
JO - Journal of microbiology and biotechnology
DO - 10.4014/jmb.2602.02040
UR - https://europepmc.org/article/MED/42894963
AB - 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.
SN - 1017-7825
SN - 1738-8872
ER -