Toll-like receptor 3 and interleukine 1beta expression in circulating progenitor cells isolated from patients with hypertension and rheumatoid arthritis

Background.
Circulating progenitor cells (CPCs), including CD34+ cells and endothelial progenitor cells (EPCs), play a role in delaying atherosclerosis and cardiovascular disease. Toll-like receptor 3 (TLR3), a member of the pathogen recognition receptors
that mediates immune response and activates inflammatory
genes, is involved in the development of atherosclerosis. TLR3 has been recently detected in EPCs and its “in vitro” activation appears to induce cytokine expression and apoptosis. We measured the expression of TLR3 and Interleukine1b-mRNA in CPCs isolated from patients with high and low grade chronic inflammatory stimuli.
The aim was to evaluate whether systemic inflammation is associated with CPC number and CPC expression ofTLR3 and IL-1b.
methods. CD34+ cells were isolated from peripheral blood of 41
untreated hypertensives with left ventricular hypertrophy and carotid atherosclerosis, from 21untreated patients with rheumatoid arthritis (RA) and from 62 matched controls.TLR3 and IL-1b- RNA expression were measured in enriched sample of CD34+ cells. Plasma C-reactive protein (CRP) and fibrinogen levels were also measured.
Results. With respect to controls, CD34+ cell number was higher
in hypertensives and lower in RA. CRP and fibrinogen levels were
higher in patients than in controls but the highest value were measured in RA. TLR3-mRNA expression was not changed in hypertensives with respect to controls while it was significantly higher in RA. IL-1b-RNA expression was increased in both groups of patient but RA had highest value. CRP and fibrinogen levels were associated with IL-1b e TLR3 expression; moreover, the increased expression of IL-1b was associated with lowering CPC number.
Conclusions. The modifications induced by the low grade inflammation in hypertensives on TLR3 and IL-1b appear do not affect directly CPCs; the higher inflammatory grade in RA is associated to an increased expression of TLR3 and of IL-1b in CPCs, which appear to influence CPCs reduction.