title: Serum levels of the Th1 chemoattractant interferon-gamma-inducible protein (IP) 10 are elevated in patients with essential hypertension.
abstract: Growing evidence shows that inflammation has a pivotal role in the pathophysiology of essential hypertension (EH). Although it has been acknowledged that target organ damage involves an inflammatory response, most work has focused on the role of macrophages, but T lymphocytes have recently become the center of interest. The goal of our study was to evaluate the role of T-cell-specific cytokines in the pathogenesis of EH. The study examined 39 patients with EH (57.7±6.8 years, systolic blood pressure (SBP) 157.5±11.8 mm Hg, diastolic blood pressure 92.2±12.9 mm Hg, mean arterial pressure 113.9±12.6 mm Hg) and 30 healthy, normotensive controls (55.2±4.9 years). Blood was drawn from a peripheral vein, and serum levels of interferon-inducible protein (IP)-10 and interleukins (IL)-4, -7 and -13 were measured by a multiplexing assay. Hypertensive patients had significantly higher levels of IP-10, IL-4, IL-7 and IL-13 than control subjects. When the patients were classified into tertiles according to their serum IP-10 levels (T1: 41.2-94.1 pg ml(-1); T2: 103.4-162.5 pg ml(-1); T3: 171.7-443.5 pgml(-1)), the patients classified into the highest tertile also had the highest blood pressure. In a correlation analysis, plasma IP-10 concentration was significantly associated with SBP (r=0.59, P<0.001). Furthermore, hypertensives with microalbuminuria, an early sign of hypertensive target organ damage, had the highest IP-10 levels. A stepwise multivariate regression analysis revealed IP-10 as the strongest independent predictor of SBP (P=0.01). In conclusion, our study provides new insights into the pathophysiological mechanisms in EH linking inflammation and IP-10. However, these preliminary results need to be confirmed in larger trials.
authors.affiliation: Department of Cardiology/Medical Clinic II, University of Erlangen-Nuremberg, Erlangen, Germany. ch.stumpf@web.de
authors.forename: Christian
authors.initials: C
authors.lastname: Stumpf
authors.forename: Christoph
authors.initials: C
authors.lastname: Auer
authors.forename: Atilla
authors.initials: A
authors.lastname: Yilmaz
authors.forename: Piotr
authors.initials: P
authors.lastname: Lewczuk
authors.forename: Lutz
authors.initials: L
authors.lastname: Klinghammer
authors.forename: Markus
authors.initials: M
authors.lastname: Schneider
authors.forename: Werner G
authors.initials: WG
authors.lastname: Daniel
authors.forename: Roland E
authors.initials: RE
authors.lastname: Schmieder
authors.forename: Christoph D
authors.initials: CD
authors.lastname: Garlichs
mesh_terms: D016022:Case-Control Studies; D054357:Chemokine CXCL10 / Q000097:blood*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000503:physiopathology*; D007249:Inflammation / Q000503:physiopathology*; D018793:Interleukin-13 / Q000097:blood; D015847:Interleukin-4 / Q000097:blood; D015851:Interleukin-7 / Q000097:blood; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D010865:Pilot Projects; D013601:T-Lymphocytes / Q000502:physiology
chemical_list: C114753:CXCL10 protein, human; D054357:Chemokine CXCL10; D018793:Interleukin-13; D015851:Interleukin-7; D015847:Interleukin-4