Interferon-induced protein 10 and interleukin 8 - C-X-C chemokines presentin proliferative diabetic retinopathy

Citation
Sg. Elner et al., Interferon-induced protein 10 and interleukin 8 - C-X-C chemokines presentin proliferative diabetic retinopathy, ARCH OPHTH, 116(12), 1998, pp. 1597-1601
Citations number
24
Categorie Soggetti
Optalmology,"da verificare
Journal title
ARCHIVES OF OPHTHALMOLOGY
ISSN journal
00039950 → ACNP
Volume
116
Issue
12
Year of publication
1998
Pages
1597 - 1601
Database
ISI
SICI code
0003-9950(199812)116:12<1597:IP1AI8>2.0.ZU;2-3
Abstract
Objective: To determine vitreous levels of interleukin 8 (IL-8) and interfe ron-induced protein 10 (IP-10),which are members of the C-X-C chemokine fam ily that promote and inhibit neovascularization, respectively. Methods: We measured the levels of IL-8 and IP-10 by specific enzyme-linked immunosorbent assays in the vitreous from 30 patients with proliferative d iabetic retinopathy (PDR) and 10 control patients undergoing vitrectomy for idiopathic macular holes or idiopathic macular puckers. Results: Detectable levels of IL-8 were found in 23 of 24 patients with act ive PDR, 4 of 6 patients with inactive PDR, and 6 of 10 controls. Levels of IL-8 were significantly increased in vitreous samples from the patients wi th active PDR (P=.02) when compared with vitreous samples from the controls . The IL-8 levels detected in vitreous samples from patients with inactive PDR were not significantly elevated over those found in the control samples . Interferon-induced protein 10 was detected in the vitreous samples from 2 3 of 24 patients with active PDR, all patients with inactive PDR, and 9 of 10 controls. Significant elevations of IP-IO were measured in samples from patients with active PDR (P=.004) and in those with inactive PDR (P=.00) ov er those from controls. In addition, levels of IP-10 were significantly ele vated in vitreous samples from-patients with inactive PDR compared with vit reous samples from patients with active PDR (P=.02). Conclusion: Both IL-8 and IP-10 participate in the pathogenesis of PDR.