CD14-159 and -260 gene polymorphisms are associated with HBV-related cirrhotic injury in Chinese Han patients.

The present study aimed to investigate the association between TLR4 mutations (Asp299Gly and Thr399Ile) and CD14 polymorphisms (base pair -159 and -260) with HBV-related cirrhosis in Chinese Han patients. By use of a polymerase chain reaction-based restriction fragment length polymorphism (PCR-RFLP) analysis technique, we genotyped Toll-like receptor 4 (TLR4) Asp299Gly and Thr399Ile and CD14-159 and -260 polymorphisms in 110 HBV-related cirrhotic patients and 110 healthy controls from the Chinese Han population. We found significant differences in the genotypes and allele frequencies of CD14-159 (but not -260) between healthy controls and liver cirrhotic patients, and both the CD14-159 and -260 genotypes were significantly different among Child-Pugh grades in cirrhotic patients. No TLR4 Asp299Gly and Thr399Ile mutations were detected in any cirrhotic patients or healthy controls in the Chinese Han population. These findings indicated that the polymorphisms of CD14, but not TLR4 Asp299Gly and Thr399Ile mutations, may be an important genetic factor for HBV-related cirrhotic injury in the Chinese Han population.

The significance of platelet activation in ankylosing spondylitis.

The objective of this study was to explore the significance of platelet activation in patients with ankylosing spondylitis (AS). Thirty-five AS patients and 15 normal controls were selected from November 2005 to October 2006. The number of CD62P- and CD63-positive cells were detected by flow cytometry. At the same time, the erythrocyte sedimentation rate (ESR), platelet count (PLT) and C-reactive protein (CRP) were determined in both groups. The percentage of CD62P-positive cell in AS patients (13.60 +/- 7.64%) was significantly higher than that in control group (2.78 +/- 1.04%; P < 0.01). The percentage of CD63-positive cell in AS patients (6.92 +/- 4.16%) was significantly higher than that in control group (4.13 +/- 1.85%; P < 0.05). The levels of CRP (20.18 +/- 23.17 mg/l), PLT (259.54 +/- 102.59 x 10(9)/l) and ESR (36.86 +/- 31.23 mm/h) in AS patients were higher than those in normal controls, respectively (3.21 +/- 2.18 mg/l, P < 0.01; 197.00 +/- 55.70 x 10(9)/l, P < 0.01; 12.25 +/- 5.05 mm/h, P < 0.05). Platelet activation may be a sign of AS exacerbation.

[Study on the expressions and roles of renal heat shock protein 72 and Toll-like receptor 4 in hepatorenal syndrome in rat].

OBJECTIVE: To explore the expressions and roles of renal heat shock protein 72(HSP72) and Toll-like receptor 4(TLR4) during development of hepatorenal syndrome in rat. METHODS: Following bile duct ligation (BDL), a biliary cirrhosis and hepatorenal syndrome rat model was reproduced. The blood, the renal and hepatic tissues of the rats were examined at 1, 2, 4 and 6 weeks (6 rats were used in each week) after BDL. Blood was withdrawn from the femoral vein and centrifuged. The plasma concentrations of alanine aminotransferase (ALT), total bilirubin (TBil), blood urea nitrogen (BUN) and creatinine (Cr) were measured, and those of the HSP72 and tumor necrosis factor-alpha (TNF-alpha) were assessed with enzyme linked immunosorbent assay (ELISA). After weighing liver and kidney and expressions of HSP72 and TLR4 in renal tissue were determined by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting. All data were compared with control group (C group). RESULTS: The plasma levels of ALT, TBil at each week and of BUN, Cr at 4 and 6 weeks were increased significantly (all P<0.05). The concentration of plasma HSP72 and the expressions of renal HSP72 mRNA and protein were lower (especially at 4 and 6 weeks, both P<0.01) in BDL rats compared with sham operation rats. But the plasma TNF-alpha levels and renal TLR4 (mRNA and protein) expressions were significantly higher than those of sham operation rats (all P<0.01). CONCLUSION: Decreased expression of renal HSP72 may contribute to activate the TLR4- initiating inflammatory signal pathway, attributing partly to the pathogenesis of hepatorenal syndrome in biliary cirrhosis.

The significance of platelet activation in rheumatoid arthritis.

We evaluated the significance of platelet activation in patients with rheumatoid arthritis (RA). The expression of CD62P and CD63 by platelets was determined using flow cytometry in 18 active RA patients, 10 remission RA and 15 normal controls. Meanwhile, the erythrocyte sedimentation rate (ESR) and C-reactive protein was also determined in all groups. The expression of CD62P in active RA patients (11.88 +/- 2.47%) was significantly higher than that in remission RA group (2.85 +/- 1.60%; P < 0.01) and control group (2.78 +/- 1.04%; P < 0.01). The expression of CD63 in active RA patients (9.90 +/- 3.02%) was significantly higher than that in remission RA group (4.11 +/- 2.00%; P < 0.01) and control group (4.13 +/- 1.85%; P < 0.01). The level of CRP (54.33 +/- 23.35 mg/l) and ESR (86.06 +/- 33.67 mm/h) in active RA patients was higher than that in remission RA group (2.55 +/- 1.01 mg/l, 14.70 +/- 4.57 mm/h; P < 0.01 for both) and normal control group (3.21 +/- 2.18 mg/l, 12.25 +/- 5.05 mm/h; P < 0.01 for both). There was a positive correlation between CD62P and ESR (r = 0.5224, P < 0.01) and also a positive correlation between CD62P and CRP (r = 0.7048, P < 0.01) as well as between CD63 and ESR (r = 0.4476, P < 0.05) but no correlation between CD63 and CRP. Platelet activation may be a sign of RA exacerbation.

[The experimental study on the expression of toll-like receptor 2 in fulminant hepatic failure].

OBJECTIVE: In order to explore the role of toll-like receptors 2 (TLR2) in initiating inflammatory response, the expression of TLR2 of the liver and IL-18, TNF-alpha and IFN-gamma of plasma in fulminant hepatic failure was analysed. METHODS: D-galactosamine (D-Gal, 900 mg/kg) and lipopolysaccharide (LPS, 10 microg/kg) were administered intraperitoneally into the BALB/C mice. To evaluate the hepatic injury, serum transaminase (ALT and AST) and plasma IL-18, TNF-alpha and IFN-gamma were determined and the mortality was observed at various time points following the intraperitoneal injection. The level of TLR2 mRNA was measured by semiquantitative RT-PCR. The protein expression of TLR2 in the liver was detected by immunohistochemistry. The data was analyzed by SAS software. RESULTS: After 4 hours of intraperitoneal injection of D-Gal/LPS, the serum transaminase and plasma IL-18, TNF-alpha and IFN-gamma levels were elevated. The treated mice began to die at 7 hours. The mortality reached up to 80% at 10 h. TLR2 mRNA was expressed at a low level in liver tissues of normal mice, while it was significantly increased and maintained at a higher level following intraperitoneal injection with D-Gal/LPS. The expression of TLR2 protein was similar to that of the TLR2 mRNA, and the expression of TLR2 mRNA was positively correlated with the concentration of plasma IL-18, TNF-alpha and IFN-gamma (r=0.36, P=0.02; r = 0.48, P 0.003; r = 0.72, P<0.001) at different time points. CONCLUSIONS: Our results showed that TLR2 was involved in initiating and inducing the expression of proinflammation cytokines in this model of fulminant hepatic failure. The results suggest that adjusting the expression of TLR2 might be a new strategy in preventing the development of infectious diseases