TNF-α/IL-1β/IL-1α/IL-12 inflammatory cytokine axes coupled with TLR1/TLR3/TLR5/MYD88 immune signaling pathway over-activation contribute to simultaneous carotid and coronary artery and occlusion in elderly patients.

Background: It remains difficult to evaluate the risk factors for concomitant carotid artery as well as coronary artery diseases in elderly patients. The aim of this research was to determine the TNF-α/IL-1β/IL-1α/IL-12 axes-TLR1/TLR3/TLR5/MYD88 immune signaling pathway interactions in coexistent carotid artery occlusion and coronary artery occlusion in elderly patients.
Methods: Elderly patients, who underwent carotid ultrasonography and coronary computed tomography angiography, were consecutively included in this research. The analyzed groups consisted of those with coexistent carotid artery occlusion and coronary artery occlusion as well as healthy individuals were enrolled as control group. The circulating levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-1α (IL-1α), interleukin-12 (IL-12), toll-like receptor 1 (TLR1), toll-like receptor 3 (TLR3), toll-like receptor 5 (TLR5) and myeloid differentiation factor 88 (MYD88) were measured.
Results: The biomarkers (TNF-α, IL-1β, IL-1α, IL-12, TLR1, TLR3, TLR5 and MYD88) were significantly increased in carotid artery occlusion + left circumflex coronary artery occlusion group when compared with control group and carotid artery occlusion + right coronary artery occlusion group, respectively (P < 0.001), and were further elevated in carotid artery occlusion + left anterior descending coronary artery occlusion group when compared to carotid artery occlusion + right coronary artery occlusion group and carotid artery occlusion + left circumflex coronary artery occlusion group, respectively (P < 0.001).
Conclusion: This research demonstrated that the TNF-α/IL-1β/IL-1α/IL-12 axes and TLR1/TLR3/TLR5/MYD88 immune signaling pathway implicated in the pathogenesis of carotid artery occlusion with coronary artery occlusion in elderly patients.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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