Background: This study was to investigate the expression of toll-like receptor 2 and its downstream effectors in endothelial cells in response to the serum from maintenance hemodialysis (MHD) patients with acute coronary syndrome (ACS).
Methods: Human renal glomerular endothelial cells (HRGEC) were treated in vitro with serum from the healthy subjects (control group), the MHD patients with stable angina pectoris (SAP group), or the MHD patients with ACS (ACS group). The cells in ACS group were cultured in the presence or absence of TLR2 signaling blockers for 18 h. The mRNA level for TLR2, nuclear factor-κB (NF-κB), interleukin-6 (IL-6) and vascular cell adhesion molecule-1 (VCAM-1) were examined by real-time qPCR, the localization of TLR2 was detected by immunocytochemistry, and the secretion of IL-6 and VCAM-1 were measured by enzyme-linked immunosorbent assay.
Results: The mRNA level of TLR2, NF-κB and IL-6 were statistically higher in the ACS group when compared with those in SAP group and healthy controls (p < 0.05), but not significantly different between SAP and healthy controls. The secretion of IL-6 in ACS group was increased when compared with SAP group and control subjects (p < 0.05). When the HRGEC were cultured with the anti-TLR2 antibodies, the expression of NF-κB, IL-6 and VCAM-1 mRNA as well as the secretion of IL-6 and VCAM-1 were significantly inhibited (p < 0.05).
Conclusion: This study revealed that the TLR2 signaling may mediate pro-inflammatory response in the MHD patients occurring with ACS.
Keywords: Acute coronary syndrome; end-stage renal disease; hemodialysis; inflammation; toll-like receptor 2.