Chemokine CCL2 from proximal tubular epithelial cells contributes to sepsis-induced acute kidney injury
Ping Jia, Sujuan Xu, Xiaoyan Wang, Xiaoli Wu, Ting Ren, Zhouping Zou, Qi Zeng, Bo Shen, Xiaoqiang Ding
Abstract
This study provides a mechanistic insight into how C-C motif chemokine ligand 2 (CCL2) is upregulated in renal tubular epithelial cells (TECs) and contributes to kidney dysfunction during sepsis. The data reveal that lipopolysaccharide induces CCL2 expression through the Toll-like receptor 2/NF-κB signaling pathway in TECs. Endogenous CCL2 released from TECs, not from myeloid cells, is responsible for sepsis-induced kidney inflammation and acute kidney injury.
Topics & Concepts
SepsisChemokineAcute kidney injuryCCL2LipopolysaccharideKidneyDownregulation and upregulationMyeloid cellsInflammationMedicineCCR2Chemokine receptorCancer researchCell biologyImmunologyMyeloidBiologyInternal medicineGeneBiochemistryImmune Response and InflammationImmune cells in cancerSepsis Diagnosis and Treatment