CD8+ T lymphocytes regulate the arteriogenic response to ischemia by infiltrating the site of collateral vessel development and recruiting CD4+ mononuclear cells through the expression of interleukin-16. (1/10)

BACKGROUND: Previous studies have demonstrated that macrophages and CD4+ T lymphocytes play pivotal roles in collateral development. Indirect evidence suggests that CD8+ T cells also play a role. Thus, after acute cerebral ischemia, CD8+ T cells infiltrate the perivascular space and secrete interleukin-16 (IL-16), a potent chemoattractant for monocytes and CD4+ T cells. We tested whether CD8+ T lymphocytes contribute to collateral vessel development and whether the lack of circulating CD8+ T cells prevents IL-16 expression, impairs CD4+ mononuclear cell recruitment, and reduces collateral vessel growth after femoral artery ligation in CD8(-/-) mice. METHODS AND RESULTS: After surgical excision of the femoral artery, laser Doppler perfusion imaging demonstrated reduced blood flow recovery in CD8(-/-) mice compared with C57/BL6 mice (ischemic/nonischemic limb at day 28, 0.66+/-0.04 versus 0.87+/-0.04, respectively; P<0.01). This resulted in greater calf muscle atrophy (mean fiber area, 785+/-68 versus 1067+/-69 microm2, respectively; P<0.01) and increased fibrotic tissue content (10.8+/-1.2% versus 7+/-1%, respectively; P<0.01). Moreover, CD8(-/-) mice displayed reduced IL-16 expression and decreased CD4+ T-cell recruitment at the site of collateral vessel development. Exogenous CD8+ T cells, infused into CD8(-/-) mice immediately after femoral artery ligation, selectively homed to the ischemic hind limb and expressed IL-16. The restoration of IL-16 expression resulted in significant CD4+ mononuclear cell infiltration of the ischemic limb, faster blood flow recovery, and reduced hindlimb muscle atrophy/fibrosis. When exogenous CD8+ T cells deficient in IL-16 (IL-16(-/-)) were infused into CD8(-/-) mice immediately after femoral artery ligation, they selectively homed to the ischemic hind limb but were unable to recruit CD4+ mononuclear cells and did not improve blood flow recovery. CONCLUSIONS: These results demonstrate that CD8+ T cells importantly contribute to the early phase of collateral development. After femoral artery ligation, CD8+ T cells infiltrate the site of collateral vessel growth and recruit CD4+ mononuclear cells through the expression of IL-16. Our study provides further evidence of the significant role of the immune system in modulating collateral development in response to peripheral ischemia.  (+info)

Association between serum adiponectin levels and arteriolosclerosis in IgA nephropathy patients. (2/10)

OBJECTIVE: Adiponectin has attracted great attention because of its anti-atherogenic properties; however, to date the relationship between serum adiponectin and arteriolosclerosis has not been reported. In our study, we aimed to examine whether or not serum adiponectin levels are associated with arteriolosclerosis in patients with IgA nephropathy which is the most common form of chronic glomerulonephritis. MATERIALS AND METHODS: We enrolled 35 patients aged 35.0+/-14.6, who underwent renal biopsy from August 2004 to February 2006 in our hospital, and were confirmed to have IgA nephropathy. We examined serum adiponectin, high-sensitive C-reactive protein, total cholesterol and triglyceride level, urinary protein excretion, body mass index (BMI), and the presence of arteriolosclerosis in the renal specimens. Since the serum adiponectin level is strongly affected by renal function, we classified the patients by creatinine clearance. RESULTS: Multiple regression analysis showed the associations of adiponectin with creatinine clearance (p<0.001), BMI (p<0.001), serum triglyceride (p=0.001) and urinary protein excretion (p=0.001). We observed a positive relation of adiponectin with urinary protein excretion and an inverse relation of adiponectin with creatinine clearance, serum triglyceride, and BMI. We could not detect any relation between the presence of arteriolosclerosis and adiponectin in the IgA nephropathy patients as a whole; however, in patients whose creatinine clearance was 90-120 ml/min/1.73 m2, the serum adiponectin level of patients with arteriolosclerosis was lower than in those without arteriolosclerosis (p=0.025). CONCLUSION: The serum level of adiponectin was related to arteriolosclerosis in IgA nephropathy patients whose renal function was almost normal. Adiponectin may prevent renal arteriolosclerosis.  (+info)

Lead, at low levels, accelerates arteriolopathy and tubulointerstitial injury in chronic kidney disease. (3/10)

Chronic lead exposure has been epidemiologically linked with hypertension and renal disease. Clinical studies suggest that low lead levels may contribute to renal progression. However, experimental studies have not examined whether low levels of lead accelerate progression in experimental chronic renal disease. Sprague-Dawley rats were administered lead (L; 150 ppm in drinking water, n = 16) for 4 wk, followed by remnant kidney (RK) surgery with continuation of lead for an additional 12 wk; control rats (n = 9) were treated similarly but did not receive lead. Lead treatment was well tolerated and resulted in modest elevations in whole blood lead levels (26.4 +/- 4.5 vs. 1 +/- 0 mug/dl, week 16, P < 0.001). Lead treatment was associated with higher systolic blood pressure (P < 0.05) and worse renal function (creatinine clearance 1.4 +/- 0.4 vs. 1.8 +/- 0.5 ml/min, RK+L vs. RK, P < 0.05), and with a tendency for greater proteinuria (6.6 +/- 6.1 vs. 3.6 +/- 1.5 mg protein/mg creatinine, RK+L vs. RK, P = 0.08). While glomerulosclerosis tended to be worse in lead-treated rats (37.6 +/- 11 vs. 28.8 +/- 2.3%, RK+L vs. RK, P = 0.06), the most striking finding was the development of worse arteriolar disease (P < 0.05), peritubular capillary loss (P < 0.05), tubulointerstitial damage, and macrophage infiltration (P < 0.05) in association with significantly increased renal expression of monocyte chemoattractant protein-1 mRNA. In conclusion, lead accelerates chronic renal disease, primarily by raising blood pressure and accelerating microvascular and tubulointerstitial injury.  (+info)

Apo B/Apo A-I ratio in central and peripheral arterial diseases. (4/10)

BACKGROUND: The apo B/apo A-I ratio represents the balance between atherogenic particles, rich in apo B, and the antiatherogenic ones, apo A-I rich. This study investigated the association between atherosclerotic diseases in different anatomical sites and apo B/apo A-I ratio. METHODS: Lipids, lipoproteins, and apolipoproteins A-I and B were assessed in 30 subjects with coronary artery disease (CAD), 26 with ischemic stroke (IS), 30 with peripheral arterial obstructive disease (PAOD), and 38 healthy subjects (controls). RESULTS: HDLc and Apo A-I were significantly lower in PAOD and CAD groups, respectively, than in other groups. Significantly higher levels of triglycerides were observed for CAD and PAOD groups than for controls. Apo B was significantly higher in IS group than in control and PAOD groups. The apo B/apo A-I ratio showed significantly higher in CAD and IS groups when compared to control and PAOD groups (p < 0.001). CONCLUSION: The apo B/apo A-I ratio was important for identifying an increased trend for coronary and cerebral atherosclerosis. In spite of the increased trend for apo B/apo A-I ratio in IS and CAD groups, the studied variables cannot be considered in an isolated way, given as those parameters were analyzed together by a binary logistic regression, no association has been demonstrated.  (+info)

Cholesterol-lowering effect of kori-tofu protein and its high-molecular-weight fraction content. (5/10)

The serum total cholesterol concentration was significantly lower in the kori-tofu feeding group than in the soy protein isolate (SPI) group, except on the 28th day of the experiment. The high-molecular-weight fraction (HMF) content of the kori-tofu protein was significantly higher than that of SPI. This difference in the HMF content may have influenced the cholesterol-lowering effect of the protein.  (+info)

Chronic kidney disease, severe arterial and arteriolar sclerosis and kidney neoplasia: on the spectrum of kidney involvement in MELAS syndrome. (6/10)

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Serum complement C3 predicts renal arteriolosclerosis in non-diabetic chronic kidney disease. (7/10)

AIM: Complement C3 (C3) is one of the major mediators of inflammation. Serum C3 has been shown to be correlated with the presence of atherosclerosis. We examined whether the serum C3 level might be correlated with the severity of renal arteriolosclerosis in patients with chronic kidney disease (CKD). METHODS: Non-diabetic CKD (stages 1-3) patients who underwent renal biopsy were enrolled in this study. Renal arteriolosclerosis was defined by the presence of hyaline changes and vessel wall thickening in the renal biopsy specimens. We examined whether the serum C3 level might be correlated with the severity of renal arteriolosclerosis in CKD patients. RESULTS: A total of 208 CKD patients (age 36.0+/-13.6 years; 94 male) who underwent renal biopsy were included. Univariate analysis showed that the serum C3 level was positively correlated with age, body mass index, blood pressure and the serum triglyceride, LDL cholesterol and CRP (p<0.001). The serum C3 level was also inversely correlated with serum HDL cholesterol (p<0.001). Multiple regression analysis identified that the serum C3 (p=0.043) as well as age (p<0.001), serum uric acid (p=0.009) and eGFR (p= 0.025) were independently associated with the severity of renal arteriolosclerosis. CONCLUSION: Our results suggest that the serum C3 level is a reliable marker of renal arteriolosclerosis. Components of metabolic syndrome were also correlated with the serum C3 level. Inflammation or metabolic syndrome may contribute to CKD through influencing the rate of progression of renal arteriolosclerosis.  (+info)

Relationship of red splenic arteriolar hyaline with rapid death: a clinicopathological study of 82 autopsy cases. (8/10)

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