Sepsis has poor prognosis, and its pathogenesis is not clear. Chemokine CX3CL1 (Fractalkine, FNK) has many functions such as chemotaxis, adhesion and mediate immune injury. CX3CR1 is the only receptor of CX3CL1 and participates in the development of sepsis. Here we review the structure, biological function and possible mechanism of CX3CL1 and CX3CR1 in the pathogenesis of sepsis.

Objective To evaluate the clinical utility of CMV pp65 antigenemia by CMV brite Kit for predicting active/reactive CMV infection S as well as of CMV diseases in bone marrow or peripheral stem cell transplant patients. We also investigated the efficacy of preemptive therapy guided by detection of CMV antigenemia. Methods A total of 210 EDTA anticoagulant plasma samples from 36 bone marrow or Peripheral Stem Cell Transplant Patients were prospectively collected from September 1999 to April 2000. The specific CMV antibody IgG/IgM of all patients were detected by ELISA. We detected CMV pp65 antigenemia by indirect immunofluorescence assay using CMV Brite Kit. All blood samples were detected weekly from week 3 after bone marrow transplantation until 100 days or antigenemia turning negative/dischage or death. Ganciclovir preemptive therapy was initiated at first positive pp65 antigenemia. Results Of 36 bone marrow or Peripheral Stem Cell Transplant Patients, 16 patients occurred positive pp65 antigenemia, 15 patients suffered from symptomatic CMV infections or CMV diseases. In 14 patients of positive pp65 antigenemia receiving gaciclovir therapy at first antigenemia, 2 patients died (mortality rate 14.2%), 12 patients of pp65 antigenemia became negative. Otherwise, 2 untreated cases died. The study showed a significant difference in mortality rate between treated and untreated patients (P

Objective To investigate the effect of artemisinin on the proliferation of human hepatoma cell line HepG‐2 .Methods The inhibition effect of cell proliferation in human hepatocelluar carcinoma cell line HepG2 of artemisinin was detected by MTT test ,and the cell cycle and apoptosis were detected by Flow cytometry .Results Artemisinin at 80 umol/L could effectively inhibi‐ted the proliferation of HepG‐2 cell in a dose‐and time‐dependent manner;the drugs could block cells at G0/S phase ,and induct the HepG‐2 cell apoptosis .Conclusion Artemisinin could effectively inhibit the proliferation of HepG‐2 cell .

OBJECTIVEThe aim of this study was to survey the influence of Toll-like receptor 2 (TLR2) and Toll-like receptor 4 (TLR4) repression to receptor activator of nuclear factor-kappaB ligand (RANKL) expression of human periodontal ligament fibroblasts (HPDLFs) under the stimulation of lipopolysaccharide (LPS).

METHODSThe level of RANKL in HPDLFs stimulated by 100 ng x mL(-1), 1 microg x mL(-1) and 10 microg x mL(-1) Escherichia coli (E. coli) LPS after 6, 12, 24 and 48 h was detected by enzyme linked immunosorbent assay (ELISA). The level of RANKL in HPDLFs stimulated by 1 microg x mL(-1) E. coli LPS after pretreatment with different titre anti-TLR2+anti-TLR4, anti-TLR2 and anti-TLR4 antibody were observed respectively.

RESULTSRANKL was detected at 6 h after stimulation with LPS, and the levels of these cytokine were highest at 24 h, and then gradually decreased. The regularity of each LPS concentration was approximately similar. After pretreatment with anti-TLR2+anti-TLR4, anti-TLR2 and anti-TLR4 antibody, the level of RANKL was significantly decreased under the stimulation of 1 microg x mL(-1) LPS (P<0.05). In the three groups, the expression of RANKL was significantly different (P<0.05). The level of RANKL in anti-TLR2+anti-TLR4 antibody pretreatment group was the lowest, the level in anti-TLR4 antibody pretreatment group was higher, and the level in anti-TLR2 antibody pretreatment group was the highest.

CONCLUSIONTLR2 and TLR4 participate in the process of RANKL expres-in HPDLFs induced by LPS. Anti-TLR4 antibody has better inhibition effect to RANKL expression of HPDLFs stimulated by LPS than anti-TLR2.

Escherichia coli ; Fibroblasts ; Humans ; Lipopolysaccharides ; Periodontal Ligament ; RANK Ligand ; Toll-Like Receptor 2 ; Toll-Like Receptor 4

OBJECTIVETo investigate the expression of fractalkine (FKN) in the blood and renal tissues of patients with lupus nephritis and explore its significance.

METHODSAccording to the pathological classification, 48 patients with lupus nephritis were divided into mild group (22 cases) and severe group (26 cases), with 26 healthy subjects as the control group. RT-PCR and enzyme-linked immunosorbent assay were employed to detect the expression of FKN mRNA and protein in the blood of the subjects, and FKN expression and localization in the renal tissue of the patients with lupus nephritis were detected using immunohistochemical staining.

RESULTSThe patients in both the mild and severe groups showed significantly increased expression of blood FKN mRNA and protein compared with the normal controls, and the increase was more obvious in severe cases (P<0.01). In the renal tissues of the patients, FKN was located mainly in the cytoplasm of the glomerular podocytes and renal tubular epithelial, and the number of positive glomerular cells number was significantly greater in severe cases than in the mild cases (P<0.01); FKN expression in the cortical interstitium did not show a significant difference between the 3 groups.

CONCLUSIONFKN expression in the blood and glomeruli of patients with lupus nephritis is related to the severity of renal pathologies.

Adult ; Case-Control Studies ; Chemokine CX3CL1 ; blood ; metabolism ; Female ; Humans ; Kidney ; metabolism ; Lupus Nephritis ; blood ; metabolism ; Middle Aged

Objective To investigate the effect of miR-142-3p on the apoptosis of rat pancreatic exocrine cell line AR42J by regulating Hmgb1.Methods AR42J cells were divided into blank group(blank),acute pancreatitis model group(AP,100 nmol/L cerulein for 24 h),and then transfected with miR-142-3p mimics,mimics NC,miR-142-3p inhibitor and inhibitor NC,respectively.The cells in the model group were recorded as miR-142-3p mimics group,mimics NC group,miR-142-3p inhibitor group and inhibitor NC.The expression of miR-142-3p in cells was detected by RT-qPCR.The protein expressions of HMGB1,caspase-3,Bax and Bcl-2 were detected by Western blot.Hoechst staining was used to determine cell apoptosis.The apoptosis rate of cells was detected by flow cytometry.The targeting relationship between miR-142-3p and Hmgb1 was determined by dual luciferase reporter gene assay.Results Compared with blank control group,the expression level of miR-142-3p in the AP group was significantly down-regulated(P＜0.01),the expression level of HMGB1 and caspase-3 proteins was up-regulated(P＜0.05),the expression level of Bax protein was significantly up-regulated(P＜0.01),the expression level of Bcl-2 protein was significantly decreased(P＜0.01)and the apoptosis rate increased significantly(P＜0.01).Compared with the mimics NC group,the level of miR-142-3p in the miR-142-3p mimics group was significantly up-regulated(P＜0.01),the expression of HMGB,caspase-3 and Bax proteins was significantly down-regulated(P＜0.01),the expression of Bcl-2 protein was up-regulated(P＜0.05),and the apoptosis rate decreased signifi-cantly(P＜0.01).Compared with inhibitor NC group,the expression level of miR-142-3p in miR-142-3p inhibitor group was down-regulated(P＜0.05),the expression levels of HMGB1,caspase-3 and Bax proteins were signifi-cantly up-regulated(P＜0.01),the expression level of Bcl-2 protein was decreased(P＜0.05)and the apoptosis rate increased significantly(P＜0.01).The dual luciferase reporter gene assay showed that Hmgb1 was the target gene of miR-142-3p.Conclusions 1)The expression of miR-142-3p was low in the model group.2)miR-142-3p can inhibit the apoptosis of AR42J cells by inhibiting the expression of Hmgb1.