Immune-cell imbalance and immunometabolic reprogramming in chronic prostatitis/chronic pelvic pain syndrome
- 1Department of Urology, The First Affiliated Hospital of Anhui Medical University , ,
Abstract
Available evidence suggests that disruption of immune homeostasis may contribute to chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) beyond the effects of localized infection. This narrative review uses immune cells as its organizing axis and synthesizes recent evidence from single-cell sequencing, Mendelian randomization, and multi-omics. The available findings suggest that the M1/M2 dichotomy may not fully capture macrophage heterogeneity in prostatic tissues and that activation of the NLRP3 inflammasome and IL-1β release may form a candidate link between innate immunity and the Th17 response. On this basis, the review discusses how glycolytic and oxidative-stress-related reprogramming may shape immune-cell states; considers chemokine networks such as CCL5/CCR5 and CXCL10/CXCR3 in the recruitment of macrophages, Th1 cells, and Th17 cells to prostatic tissue; and examines how mast cells and neurogenic inflammation may participate in the bidirectional neuro-immune dialogue associated with persistent pain. At the intervention level, we distinguish human clinical observations and interventions from findings in cell systems and animal models, and discuss candidate strategies involving the NLRP3 inflammasome, chemokine receptors, microbiota-derived metabolites, neuromodulation, and local or multi-component approaches. These concepts require prospective validation in clinically defined CP/CPPS subgroups before they can support mechanism-guided treatment.
Related
- The p38 MAPK/MSK1/NF-κB axis in chronic prostatitis/chronic pelvic pain syndrome: a testable hypothesis for innate immune inflammatory amplification
- Redox Storm in the Tumor Microenvironment (ΤΜΕ): Multifaceted Redox Injury and Immunometabolic Reprogramming Induced by Immune Checkpoint Blockade in B16F10 Melanoma: An Ultrastructural Study of the Peritumoral Interface
- Unveiling the missing link between chronic prostatitis and prostate cancer: emerging roles of exosomal miRNAs as extracellular vesicle messengers
- Nanotherapeutic macrophage reprogramming through immunometabolic and microbial modulation for sepsis treatment.
- The IFN-γ-inducible GTPase IIGP1 regulates mitochondrial remodeling and immunometabolic reprogramming during inflammatory macrophage polarization
BibTeX
@article{li2026immunecell,
title = {{Immune-cell imbalance and immunometabolic reprogramming in chronic prostatitis/chronic pelvic pain syndrome}},
author = {Hao Li and Andong Cheng and Mengfan Wang and Shiyang Zhou and Xixi Wang and Xingchi Zhu and Kun Wang and Yu Guan and Jialin Meng and Chaozhao Liang},
journal = {Frontiers in immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.1926409},
url = {https://europepmc.org/article/PMC/PMC13673328},
note = {CC BY},
}
RIS
TY - JOUR
TI - Immune-cell imbalance and immunometabolic reprogramming in chronic prostatitis/chronic pelvic pain syndrome
AU - Hao Li
AU - Andong Cheng
AU - Mengfan Wang
AU - Shiyang Zhou
AU - Xixi Wang
AU - Xingchi Zhu
AU - Kun Wang
AU - Yu Guan
AU - Jialin Meng
AU - Chaozhao Liang
PY - 2026
DA - 2026/10/02
JO - Frontiers in immunology
DO - 10.3389/fimmu.2026.1926409
UR - https://europepmc.org/article/PMC/PMC13673328
AB - Available evidence suggests that disruption of immune homeostasis may contribute to chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) beyond the effects of localized infection. This narrative review uses immune cells as its organizing axis and synthesizes recent evidence from single-cell sequencing, Mendelian randomization, and multi-omics. The available findings suggest that the M1/M2 dichotomy may not fully capture macrophage heterogeneity in prostatic tissues and that activation of the NLRP3 inflammasome and IL-1β release may form a candidate link between innate immunity and the Th17 response. On this basis, the review discusses how glycolytic and oxidative-stress-related reprogramming may shape immune-cell states; considers chemokine networks such as CCL5/CCR5 and CXCL10/CXCR3 in the recruitment of macrophages, Th1 cells, and Th17 cells to prostatic tissue; and examines how mast cells and neurogenic inflammation may participate in the bidirectional neuro-immune dialogue associated with persistent pain. At the intervention level, we distinguish human clinical observations and interventions from findings in cell systems and animal models, and discuss candidate strategies involving the NLRP3 inflammasome, chemokine receptors, microbiota-derived metabolites, neuromodulation, and local or multi-component approaches. These concepts require prospective validation in clinically defined CP/CPPS subgroups before they can support mechanism-guided treatment.
SN - 1664-3224
ER -