Toll-like receptors in giant cell arteritis

Ma-Krupa, Wei; Kwan, Mildred; Goronzy, Jörg J.; Weyand, Cornelia M.

doi:10.1016/j.clim.2005.02.009

Cited by 62 publications

(40 citation statements)

References 86 publications

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“…67 Besides chronic rejection, it is noteworthy that adventitial lymphoid neogenesis has also been evidenced in inflammatory arteritis such as Kawasaki disease, 68 Takayasu 69 and giant cell arteritis. 70 …”

Section: Adventitial Lymphoid Neogenesis In Chronic Rejectionmentioning

confidence: 99%

Topological Determinants and Consequences of Adventitial Responses to Arterial Wall Injury

Michel

Thaunat

Houard

et al. 2007

ATVB

178

151

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Abstract-Arteries are composed of 3 concentric tissue layers which exhibit different structures and properties. Because arterial injury is generally initiated at the interface with circulating blood, most studies performed to unravel the mechanisms involved in injury-induced arterial responses have focused on the innermost layer (intima) rather than on the outermost adventitial layer. In the present review, we focus on the involvement of the adventitia in response to various types of arterial injury leading to vascular remodeling. Physiologically, soluble vascular mediators are centrifugally conveyed by mass transport toward the adventitia. Moreover, in pathological conditions, neomediators and antigens can be generated within the arterial wall, whose outward conveyance triggers different patterns of local adventitial response. Adventitial angiogenesis, immunoinflammation, and fibrosis sequentially interact and their net balance defines the participation of the adventitial response in arterial pathology. In the present review we discuss 4 pathological entities in which the adventitial response to arterial wall injury participates in arterial wall remodeling. Hence, the adventitial adaptive immune response predominates in chronic rejection. Inflammatory phagocytic cell recruitment and initiation of a shift from innate to adaptive immunity characterize the adventitial response to products of proteolysis in abdominal aortic aneurysm. Adventitial sprouting of neovessels, leading to intraplaque hemorrhages, predominates in atherothrombosis. Adventitial fibrosis characterizes the response to mechanical stress and is responsible for the constrictive remodeling of arterial segments and initiating interstitial fibrosis in perivascular tissues. These adventitial events, therefore, have an impact not only on the vessel wall biology but also on the surrounding tissue.

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Section: Adventitial Lymphoid Neogenesis In Chronic Rejectionmentioning

confidence: 99%

Topological Determinants and Consequences of Adventitial Responses to Arterial Wall Injury

Michel

Thaunat

Houard

et al. 2007

ATVB

178

151

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“…1,10,11 At the same time, an HFD causes endotoxemia in humans and mice 12,13 ; also, an increased concentration of LPS induces the development of atherosclerosis. 14 In our experiment, we hypothesized that the same mechanisms might be responsible for the induction of giant cell formation.…”

Section: Serum Concentration Of Endotoxin and Il-4 And Plaque Toll-limentioning

confidence: 99%

“…LPS stimulation initiates immune reactions mediated by TLR4; these reactions result in the development of granulomatous inflammation in an animal model of GCA. 1,10,11 Because the presence of MGCs is a hallmark of GCA, we suggest that the induction of giant cell formation in atherosclerotic plaques might be initiated by the same or similar trigger mechanisms. Enhanced expression of TLRs has been described in apoEϪ/Ϫ mice and in human carotid atherosclerotic plaques.…”

mentioning

confidence: 99%

Cholate-Containing High-Fat Diet Induces the Formation of Multinucleated Giant Cells in Atherosclerotic Plaques of Apolipoprotein E−/− Mice

Samokhin

Wilson

Nho

et al. 2010

ATVB

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Objective-To determine the role of multinucleated giant cells (MGCs) in cardiovascular diseases. Methods and Results-MGCs are a hallmark of giant cell arteritis. They are also described in atherosclerotic plaques from aortic aneurysms and carotid and coronary arteries. Herein, we demonstrate that the cholate-containing Paigen diet yields many MGCs in atherosclerotic plaques of apolipoprotein EϪ/Ϫ mice. These mice revealed a 4-fold increase in MGC numbers when compared with mice on a Western or Paigen diet without cholate. Most of the MGCs stained intensively for cathepsin K and were located at fibrous caps and close to damaged elastic laminae, with associated medial smooth muscle cell depletion. During in vitro experiments, MGCs demonstrated a 6-fold increase in elastolytic activity when compared with macrophages and facilitated transmigration of smooth muscle cells through a collagen-elastin matrix. An elastin-derived hexapeptide (Val-Gly-Val-Ala-Pro-Gly [VGVAPG]) significantly increased the rate of macrophage fusion, providing a possible mechanism of in vivo MGC formation. Comparable to the mouse model, human specimens from carotid arteries and aortic aneurysms contained cathepsin K-positive MGCs. Key Words: multinucleated giant cells Ⅲ cathepsin K Ⅲ atherosclerosis Ⅲ cholate Ⅲ elastin T he presence of multinucleated giant cells (MGCs) in blood vessel walls is well described in patients with giant cell arteritis (GCA). The name of this disease reflects the presence of MGCs formed by the fusion of macrophages in inflammatory infiltrates of the arterial wall. 1,2 In atherosclerosis, MGCs have been described in plaques from aortic aneurysms and carotid and coronary arteries. 3 In 1 report, 4 CD11c-positive MGCs have been observed in advanced atherosclerotic plaques of apolipoprotein E (apoE)Ϫ/Ϫ mice receiving a "Western" high-fat diet (HFD). Conclusion-ApolipoproteinHerein, we report a mouse model that consistently generates MGCs in atherosclerotic lesions. We compared the effect of a cholate-containing Paigen diet with the widely used Western HFD and also with a Paigen diet without cholate and observed that the mice in the first group developed 4 times more cathepsin K (Ctsk)-expressing MGCs than their littermates on cholate-free HFDs. Researchers [5][6][7] have previously shown that cathepsin K is critical for the elastic lamina degradation in atherosclerotic lesions in apoEϪ/Ϫ mice. The identification of MGCs close to elastin fibers and especially in the proximity of elastin fiber breaks prompted us to investigate the effect of cathepsin K deficiency on the ability of MGCs to cleave elastin fibers and to facilitate smooth muscle cell (SMC) migration through an elastin-collagen layer. We also tested the effect of an elastin-derived hexapeptide (Val-Gly-Val-Ala-Pro-Gly [VGVAPG]) on the rate of interleukin (IL) 4 -induced fusion of thioglycolate-elicited peritoneal macrophages. Previously, it has been shown that this peptide has a diverse biological activity, including an induction of macrophage migration and agg...

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“…Other experimental data suggest that temporal arteritis is initiated in the outer layer of the arterial wall, with CD4 T cells entering the artery wall through the vasa vasorum and subsequently orchestrating macrophage differentiation [10]. The inflammatory cells then infiltrate into all layers of the artery wall, leading to myofibroblast proliferation, luminal stenosis, and tissue ischemia.…”

Section: Discussionmentioning

confidence: 99%

“…the intracranial arteries) [4,8,9]. Other experimental data suggests that the disease is initiated in the outer layer of the arterial wall, with inflammatory cells entering through the vasa vasorum and subsequently infiltrating into all layers of the artery wall [10]. …”

Section: Introductionmentioning

confidence: 99%

Studies on the Histopathology of Temporal Arteritis

et al. 2016

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Aims: The aim of this paper was to identify the location and to grade the severity of most significant inflammation within positive temporal artery biopsies along with other key clinical and histologic characteristics. Methods: Charts and pathology slides for 70 patients diagnosed with temporal arteritis at the University of Wisconsin (UW) Hospital and Clinics from 1989 to 2015 were reviewed. A subset of 48 specimens was immunostained for CD68 and graded on a scale from 0 to +++; the location of staining was recorded. Results: The most severe granulomatous inflammation was in the media and adventitia in 13% (9/70) of the biopsies; the remaining had uniform full thickness inflammation. Of the slides that were stained with CD68, 94% (45/48) were positive. In 42% (19/45), the stained cells were found mainly in the muscularis and adventitia. Seven percent (3/45) of the slides had staining solely around the internal elastic lamina, and 2% (1/45) had staining limited to the intima. Conclusions: With a few exceptions, granulomatous inflammation in positive temporal artery biopsies is most evident at the media and adventitia or is uniform throughout the layers of the artery. Our study lends support to the theory that the muscularis and adventitia may play an inciting role in the pathogenesis of temporal arteritis.

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Toll-like receptors in giant cell arteritis

Cited by 62 publications

References 86 publications

Topological Determinants and Consequences of Adventitial Responses to Arterial Wall Injury

Topological Determinants and Consequences of Adventitial Responses to Arterial Wall Injury

Cholate-Containing High-Fat Diet Induces the Formation of Multinucleated Giant Cells in Atherosclerotic Plaques of Apolipoprotein E−/− Mice

Studies on the Histopathology of Temporal Arteritis

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