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First, ELN has not only been observed in inflamed synovium but in many other chronically inflamed tissues affected by autoimmune diseases as well as chronic infections.
Reduced ATP levels have also been observed in inflamed tissue from patients with IBD [41], and non-inflamed biopsies obtained from Crohn's disease patients are more sensitive to uncoupling of oxidative phosphorylation [42].
Elevated levels of this AMP in psoriatic plaques have been published recently [6], [35] and autoinflammatory effects of the cathelicidin peptide LL-37 have been observed in inflamed skin in psoriasis [5], [11].
Increased steady-state levels of 8-oxo-dG adducts have been observed in inflamed breast cancer tissues, where malignant progression can occur [ 38], and in hepatocellular carcinoma [ 39].
Bacterial contact with the epithelium has previously been observed in inflamed intestinal samples, but it was only analysed on fixed biopsy samples.
Increased expression of E-selectin and P-selectin has been observed in inflamed joints from RA patients, with several studies showing significant elevations in soluble selectins in the serum of patients with active disease [ 7- 10].
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Similarly, S100A9 was evaluated and an increase of protein production was observed in inflamed compared with normal/reactive areas.
A strong expression of CTGF was observed in inflamed synovial tissue with RA, and none or very weak expression was recognized in samples with OA.
Finally, no remarkable expression of TIMP-2 was observed in inflamed mucosa of IBD patients, in an immunohistochemical study by Arihiro et al [ 7].
In contrast, TIMP-2-mRNA levels remained unchanged and no remarkable expression of TIMP-2 was observed in inflamed mucosa of IBD patients [ 6, 7].
Consistent with the microarray data, a significant increase of STC1 production was observed in inflamed compared with normal/reactive areas by Western blot analysis.
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