Expression of Toll-Like Receptors in Human Atherosclerotic Lesions

TLDR

Innate immune reactions against bacteria and viruses have been implicated in the pathogenesis of atherosclerosis. The study aims to explore the molecular mechanism of microbe recognition in the arterial wall by characterizing TLR expression in atherosclerotic lesions. The authors characterized TLR expression in atherosclerotic lesions. Semiquantitative PCR and immunohistochemistry revealed that TLR1, TLR2, and TLR4 are markedly upregulated in human atherosclerotic plaques, and many TLR‑expressing cells show NF‑κB nuclear translocation, indicating inflammatory activation.

Abstract

Background — Innate immune reactions against bacteria and viruses have been implicated in the pathogenesis of atherosclerosis. To explore the molecular mechanism by which microbe recognition occurs in the artery wall, we characterized the expression of toll-like receptors (TLRs), a family of pathogen pattern recognition receptors, in atherosclerotic lesions. Methods and Results — Semiquantitative polymerase chain reaction and immunohistochemical analysis demonstrated that of 9 TLRs, the expression of TLR1, TLR2, and TLR4 was markedly enhanced in human atherosclerotic plaques. A considerable proportion of TLR-expressing cells were also activated, as shown by the nuclear translocation of nuclear factor-κB. Conclusion — Our findings illustrate a repertoire of TLRs associated with inflammatory activation in human atherosclerotic lesions, and they encourage further exploration of innate immunity in the pathogenesis of atherosclerosis.