Synovial fluid sICAM-1 levels were significantly and positively c

Synovial fluid sICAM-1 levels were significantly and positively correlated with synovial fluid leukocyte counts. Soluble level of ICAM1 in sera and synovial fluid (SF) are correlated with some clinical parameters and synovial tissue expression

of ICAM1 in RA [115]. It has been shown that sICAM1 is able to bind to LFA-1 and competitively inhibit ICAM-1/LFA-1-mediated cell–cell interaction in vitro [116], albeit at concentrations much greater than those found in plasma. As a consequence, it is unlikely that sICAM1 antagonizes ICAM1/LFA-1-mediated cellular events in vivo. To the best of our knowledge, there have been no reports of the detection of ICAM1 and sICAM1 in ID and OA TMJ. Guanosine triphosphate see more (GTP) cyclohydrolase I (GCH1) was ranked 8 among the top 10 up-regulated genes in FLS treated with TNF-α (Table 1). In contrast, GCH1 was not observed among the top 10 up-regulated genes with IL-1β (it was ranked Fasudil 15; data not shown). GCH1 catalyzes the conversion of GTP to D-erythro-7,8-dihydroneopterin triphosphate, the first and

rate-limiting step in tetrahydrobiopterin (BH4) biosynthesis [117]. It has been demonstrated that GCH1 is a key modulator of peripheral neuropathic and inflammatory pain. BH4 represents an essential cofactor for the production of catecholamines, serotonin and nitric oxide [118], all of which are heavily implicated in the Fenbendazole pathogenesis of migraines [119]. After axonal injury, concentrations of BH4 rose in primary sensory neurons, owing to up-regulation of GCH1. After peripheral inflammation, BH4 also increased in dorsal root ganglia, owing to

enhanced GCH1 enzyme activity. Recently, it has been shown that carriers of a particular haplotype of GCH1 had decreased sensitivity to some experimental mechanical pain stimuli [120]. While recent data suggest a “protective” (less pain) haplotype in the GCH1 gene, other research has failed to confirm this association. To the best of our knowledge, although there have been no reports for GCH1 in joint diseases, GCH1 may be associated with pain in joint diseases. Further studies on GCH1 in joint diseases such as RA and OA are therefore necessary. IL-17 receptor B (IL17RB) was ranked 9 among the top 10 up-regulated genes in FLS treated with TNF-α (Table 1). In contrast, IL17RB was not among the top 10 up-regulated genes with IL-1β (it was ranked 16; data not shown). IL17RB is one of IL-17 receptor family members that now consist of 5 members (IL17RA, IL17RB, IL17RC, IL17RD and IL17RE). In contrast, the IL-17 ligand family comprises 6 members; IL-17A, IL-17B, IL-17C, IL-17D, IL-17E (also called IL-25) and IL-17F [121]. IL-17 typically refers to IL-17A. IL-17A is well characterized as a signature cytokine that participates in both acute and chronic inflammatory responses, while the other forms have not been widely studied [122].

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