AI Article Synopsis
- The study focuses on giant cell arteritis (GCA), a condition causing inflammation in large arteries, and investigates the role of fibroblast activation protein alpha (FAP), which is linked to inflammation and tissue changes.* -
- Plasma levels of FAP were found to be lower in GCA patients compared to those with polymyalgia rheumatica (PMR) and healthy controls, with levels decreasing further during remission and eventually rising near healthy levels during treatment-free remission.* -
- The research indicates that FAP is highly expressed in inflamed tissues of GCA patients and may play a key role in the disease's inflammatory and remodeling processes, suggesting it could be a potential target for future imaging and therapy.*
Article Abstract
Objective: Giant cell arteritis (GCA) is characterized by granulomatous inflammation of the medium- and large-sized arteries accompanied by remodeling of the vessel wall. Fibroblast activation protein alpha (FAP) is a serine protease that promotes both inflammation and fibrosis. Here, we investigated the plasma levels and vascular expression of FAP in GCA.
Methods: Plasma FAP levels were measured with enzyme-linked immunosorbent assay in treatment-naive patients with GCA (n = 60) and polymyalgia rheumatica (PMR) (n = 63) compared with age- and sex-matched healthy controls (HCs) (n = 42) and during follow-up, including treatment-free remission (TFR). Inflamed temporal artery biopsies (TABs) of patients with GCA (n = 9), noninflamed TABs (n = 14), and aorta samples from GCA-related (n = 9) and atherosclerosis-related aneurysm (n = 11) were stained for FAP using immunohistochemistry. Immunofluorescence staining was performed for fibroblasts (CD90), macrophages (CD68/CD206/folate receptor beta), vascular smooth muscle cells (desmin), myofibroblasts (α-smooth muscle actin), interleukin-6 (IL-6), and matrix metalloproteinase-9 (MMP-9).
Results: Baseline plasma FAP levels were significantly lower in patients with GCA compared with patients with PMR and HCs and inversely correlated with systemic markers of inflammation and angiogenesis. FAP levels decreased even further at 3 months on remission in patients with GCA and gradually increased to the level of HCs in TFR. FAP expression was increased in inflamed TABs and aorta of patients with GCA compared with control tissues. FAP was abundantly expressed in fibroblasts and macrophages. Some of the FAP fibroblasts expressed IL-6 and MMP-9.
Conclusion: FAP expression in GCA is clearly modulated both in plasma and in vessels. FAP may be involved in the inflammatory and remodeling processes in GCA and have utility as a target for imaging and therapeutic intervention.
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| http://dx.doi.org/10.1002/acr.25354 | DOI Listing |
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