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Peer-reviewedCC BY 4.0Cells

LPS-Induced Inflammatory Microenvironment Aggravates Urothelial Cell Damage and MAP Crystal Adhesion

  • Jia-Yi Zhang1
  • Xin-Yi Tong1
  • Run-Min Tan1
  • Zhi-Lin Yu1
  • Jian-Ming Ouyang1
  1. 1College of Chemistry and Materials Science, Jinan University, Guangzhou 510632, China
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Abstract

Magnesium ammonium phosphate (MAP) stones feature a markedly high recurrence rate. The inflammatory microenvironment contributes to MAP crystal-induced urothelial injury, yet the specific regulatory mechanisms remain unclear. In this study, MAP crystals were synthesized, and pharmacological intervention with the ROS scavenger N-acetylcysteine (NAC), the CTSB inhibitor CA-074 Me, and the NLRP3 inhibitor MCC950 was used to explore the signaling pathway through which MAP crystals induce inflammatory responses; an inflammatory model of SV-HUC-1 urothelial cells was established using lipopolysaccharides (LPSs) to observe the regulation of key molecules in the inflammatory signaling pathway and its effects on MAP crystal adhesion and cellular injury. Results showed that MAP crystals elevated intracellular ROS levels, aggravated lysosomal membrane permeabilization, triggered CTSB leakage, and activated the NLRP3 inflammasome pathway. In the LPS-induced inflammatory microenvironment, MAP crystals exacerbated cellular inflammatory responses and cell injury. Meanwhile, the expression of adhesion-related proteins, including OPN, CD44, and ICAM-1, was further upregulated, accompanied by aggravated MAP crystal adhesion. In summary, MAP crystals induced inflammation in SV-HUC-1 cells via the ROS–CTSB–NLRP3 axis, and the LPS-induced inflammatory microenvironment further amplified cellular inflammation, cell damage, and crystal adhesion. This study provides theoretical evidence supporting the pro-inflammatory effect of the inflammatory microenvironment on MAP stone formation.

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Cite

BibTeXRIS
BibTeX
@article{zhang2026lpsinduced,
  title = {{LPS-Induced Inflammatory Microenvironment Aggravates Urothelial Cell Damage and MAP Crystal Adhesion}},
  author = {Jia-Yi Zhang and Xin-Yi Tong and Run-Min Tan and Zhi-Lin Yu and Jian-Ming Ouyang},
  journal = {Cells},
  year = {2026},
  month = oct,
  doi = {10.3390/cells15211983},
  url = {https://www.mdpi.com/2073-4409/15/21/1983},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - LPS-Induced Inflammatory Microenvironment Aggravates Urothelial Cell Damage and MAP Crystal Adhesion
AU  - Jia-Yi Zhang
AU  - Xin-Yi Tong
AU  - Run-Min Tan
AU  - Zhi-Lin Yu
AU  - Jian-Ming Ouyang
PY  - 2026
DA  - 2026/10/30
JO  - Cells
DO  - 10.3390/cells15211983
UR  - https://www.mdpi.com/2073-4409/15/21/1983
AB  - Magnesium ammonium phosphate (MAP) stones feature a markedly high recurrence rate. The inflammatory microenvironment contributes to MAP crystal-induced urothelial injury, yet the specific regulatory mechanisms remain unclear. In this study, MAP crystals were synthesized, and pharmacological intervention with the ROS scavenger N-acetylcysteine (NAC), the CTSB inhibitor CA-074 Me, and the NLRP3 inhibitor MCC950 was used to explore the signaling pathway through which MAP crystals induce inflammatory responses; an inflammatory model of SV-HUC-1 urothelial cells was established using lipopolysaccharides (LPSs) to observe the regulation of key molecules in the inflammatory signaling pathway and its effects on MAP crystal adhesion and cellular injury. Results showed that MAP crystals elevated intracellular ROS levels, aggravated lysosomal membrane permeabilization, triggered CTSB leakage, and activated the NLRP3 inflammasome pathway. In the LPS-induced inflammatory microenvironment, MAP crystals exacerbated cellular inflammatory responses and cell injury. Meanwhile, the expression of adhesion-related proteins, including OPN, CD44, and ICAM-1, was further upregulated, accompanied by aggravated MAP crystal adhesion. In summary, MAP crystals induced inflammation in SV-HUC-1 cells via the ROS–CTSB–NLRP3 axis, and the LPS-induced inflammatory microenvironment further amplified cellular inflammation, cell damage, and crystal adhesion. This study provides theoretical evidence supporting the pro-inflammatory effect of the inflammatory microenvironment on MAP stone formation.
SN  - 2073-4409
ER  -