Expression of toll-like receptors in human atherosclerotic lesions: a possible pathway for plaque activation
K Edfeldt, J Swedenborg, GK Hansson, Z Yan - Circulation, 2002 - Am Heart Assoc
K Edfeldt, J Swedenborg, GK Hansson, Z Yan
Circulation, 2002•Am Heart AssocBackground—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 …
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 …
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.
Am Heart Assoc