title: [Elevated plasma concentration of IP-10 in patients with type 2 diabetes mellitus].
abstract: Recent studies have shown the important role of proinflammatory cytokines and chemokines in the pathogenesis of atherosclerosis and diabetes mellitus(DM). Interferon-inducible protein of 10 kD (IP-10/ CXCL10), a member of the C-X-C chemokine superfamily, is a potent chemoattractant for activated T lymphocytes and is reported to be involved in various disease states including atheroma plaque formation, inhibition of tumor angiogenesis and maintenance of podocyte function. However, the involvement of IP-10 in type 2 DM, especially in its vascular and renal complications, is largely unknown. To elucidate the etiopathological role of IP-10 in type 2 DM, we measured the concentrations of IP-10 together with IFN-gamma, TNF-alpha, IL-18, IL-6 and MCP-1 in plasma samples from 103 type 2 DM patients with various degrees of nephropathy. A significant difference in the plasma level of IP-10 was observed between the patients and the control subjects (183.3+/-12.5 pg/m/ vs 65.6+/-9.3 pg/ml, p<0.05). IP-10 correlated IL-18, IL-6, TNF-alpha and MCP-1. The IFN-gamma level was below the detectable range. IP-10 levels became higher with the progression of nephropathy : IP-10 levels were 148.9+/-14.5, 174.2+/-17.2 and 231.9+/-31.3 pg/m/ in patients with an urinary albumin creatinine ratio of <30, 30 to 300 and >300 microg/mg Cr, respectively. Similarly, IL-18, IL-6, MCP-1 and TNF-alpha levels in patients with overt albuminuria were significantly higher as compared with those without albuminuria (IL-18, 367.3 45.6 vs 203.5+/-17.6 pg/ml; IL-6, 1.61+/-0.26 vs 0.87+/-0.13 pg/ml; TNF-alpha, 1.83+/-0.48 vs 0.61+/-0.07 pg/ml; p<0.05, respectively) in consistent with previous reports. These results suggested that IP-10 may have an etiopathogenic role in type2 DM and diabetic nephropathy as one of the downstream effectors of proinflammatory cytokines.
authors.affiliation: Division of Nephrology, Endocrinology, and Vascular Medicine, Tohoku University Graduate School of Medicine, Miyagi, Japan.
authors.forename: Honglan
authors.initials: H
authors.lastname: Xu
authors.forename: Kenji
authors.initials: K
authors.lastname: Nakayama
authors.forename: Susumu
authors.initials: S
authors.lastname: Ogawa
authors.forename: Akira
authors.initials: A
authors.lastname: Sugiura
authors.forename: Taro
authors.initials: T
authors.lastname: Kato
authors.forename: Toshinobu
authors.initials: T
authors.lastname: Sato
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Sato
authors.forename: Sadayoshi
authors.initials: S
authors.lastname: Ito
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D054357:Chemokine CXCL10; D019743:Chemokines, CXC / Q000097:blood*; D003924:Diabetes Mellitus, Type 2 / Q000175:diagnosis* / Q000209:etiology; D003928:Diabetic Nephropathies / Q000175:diagnosis / Q000209:etiology; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D020382:Interleukin-18 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D011379:Prognosis
chemical_list: D015415:Biomarkers; D054357:Chemokine CXCL10; D019743:Chemokines, CXC; D018836:Inflammation Mediators; D020382:Interleukin-18; D015850:Interleukin-6