OBJECTIVETo investigate the relationship between atrial fibrillation (AF) and serum soluble CD163.

METHODSA total of 336 patients with heart valve disease were included in this study, including 167 with AF and 169 with sinus rhythm. The clinical data were compared between the two grops, and Logistic regression analysis was used to identify the risk factors associated with AF.

RESULTSThe levels of total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), tumor necrosis factor (TNF), interleukin-6 (IL - 6), high-sensitivity C-reactive protein (hs-CRP) and left atrial diameter (LAD) all differed significantly between the two groups (P<0.05). Serum soluble CD163 levels in AF patients were significantly higher than those in patients with sinus rhythm (P<0.05). Serum soluble CD163 was positively correlated with TNF (r=0.244, P=0.244), IL-6 (r=0.186, P=0.186), hs-CRP (r=0.183, P=0.183) and LAD (r=0.194, P=0.194) in patients with AF. Logistic regression analysis showed that LAD, IL-6, TNF, hs-CRP and CD163 were all associated with AF. ROC curve analysis showed that the area under curve of serum soluble CD163 was 0.861 in patients with AF (CI 95%: 0.820-0.901, P<0.01) with a sensitivity and a specificity of 80.8 and 76.9%, respectively.

CONCLUSIONSerum soluble CD163 level may be a risk factor for AF, and an increased soluble CD163 level may indicate active inflammation in AF patients.

Antigens, CD ; blood ; Antigens, Differentiation, Myelomonocytic ; blood ; Atrial Fibrillation ; blood ; C-Reactive Protein ; analysis ; Heart Atria ; pathology ; Humans ; Inflammation ; blood ; Interleukin-6 ; blood ; Lipoproteins, HDL ; blood ; Lipoproteins, LDL ; blood ; Receptors, Cell Surface ; blood ; Risk Factors ; Tumor Necrosis Factor-alpha ; blood

OBJECTIVESTo explore the role of TLR4 in the mechanism of hepatic ischemia/reperfusion (I/R) injury in mice.

METHODSWild-type (C3H/Heouj) mice and TLR4 deficient mice (C3H/Hej) were used to prepare the models of liver I/R injury. Partial hepatic ischemia was produced by inflow causing occlusion in the median and left lobes for 45 minutes. Blood was drawn to kill the mice at 1 hours and 3 hours after reperfusion. The blood was used to analyze aspartate aminotransferase (AST) and tumor necrosis factor-alpha (TNFalpha). TNF-alpha mRNA expression and myeloperoxidase (MPO) level in ischemic lobes was examined by northern blot and myeloperoxidase assay, respectively.

RESULTSAST levels were significantly lower in TLR4 deficient mice, compared with those in wild-type mice at both time points (661.83U/L+/-106.09U/L vs. 1215.5U/L+/- 174.03U/L, t=-6.65, P<0.01; 1145.17U/L+/-132.42U/L vs. 2958.17U/L+/-186.81U/L, t=-5.57, P<0.01). Serum TNF-alpha level was lower in TLR4 deficient mice at 3 hours after reperfusion compared with that in wild-type mice (152.39pg/ml+/-43.3 pg/ml vs. 249.12pg/ml+/-51.89pg/ml, t=-3.13, P<0.05). This difference appeared to be mediated at the gene level, since TNF-alpha mRNA expression had decreased in TLR4 deficient mice at 1 hours after reperfusion, compared with that in wild type mice (80.3+/-28.8 vs. 189.4+/-24.6, t=-3.25, P<0.05). MPO level in ischemic lobes in TLR4 deficient mice at 3 hours after reperfusion was significantly lower than that in wild type mice (F=33.49, P<0.01).

CONCLUSIONSI/R hepatic injury in TLR4 deficient mice is less than that in wild-type mice. TNF-alpha expression down-regulated at the mRNA level appears critical. These suggest that TLR4 be involved in the mechanism of hepatic ischemia/reperfusion injury in mice.

Alanine Transaminase ; blood ; Animals ; Liver ; blood supply ; metabolism ; Membrane Glycoproteins ; physiology ; Mice ; Mice, Inbred C3H ; Peroxidase ; metabolism ; RNA, Messenger ; analysis ; Receptors, Cell Surface ; physiology ; Reperfusion Injury ; etiology ; Toll-Like Receptor 4 ; Toll-Like Receptors ; Tumor Necrosis Factor-alpha ; analysis ; genetics

To study the biological characteristics of mesenchymal stem cells (MSC) from patients with myelodysplastic syndrome (MDS) and their supportive capacity for hematopoiesis in vitro, MSCs from bone marrow samples of MDS patients were isolated, cultured and expanded. Morphology, immunophenotype, osteoblasts differentiative and proliferative property of MSC and colony forming unit-fibroblast (CFU-F) were measured and analyzed. Mononuclear cells (MNC) of cord blood were plated onto a feeder layer formed by MSC of MDS patient, cells count and CFU-GM production were observed. The results showed that the culture-expanded cells from MDS patients presented a typical fibroblast-like morphology. Cells were positive for SH2 (CD105), SH3 (CD73), Thy-1 (CD90), but negative for CD34 and CD45. After induction, these cells could differentiate into osteoblasts. Their proliferative capacity and CFU-F number were similar to those of MSC from healthy donors. The total cell count and CFU-GM yield in supernatants after culture for 2 weeks were significantly lower than those of control in hematopoiesis supportive experiments in vitro (P < 0.05). It is concluded that the biological characteristics of MSC from bone marrow of MDS patients are not different from those of MSC isolated from bone marrow of normal donors, however, their capacity of hematopoiesis support in vitro are significantly weaker.
5'-Nucleotidase ; analysis ; Adult ; Aged ; Antigens, CD ; analysis ; Antigens, CD34 ; analysis ; Bone Marrow Cells ; cytology ; immunology ; Cell Differentiation ; Endoglin ; Female ; Hematopoiesis ; Humans ; Male ; Mesenchymal Stromal Cells ; cytology ; immunology ; Middle Aged ; Myelodysplastic Syndromes ; blood ; Receptors, Cell Surface ; analysis

BACKGROUNDRupture of unstable plaque with subsequent thrombus formation is the common pathophysiological substrate of acute coronary syndrome (ACS). It is of potential significance to explore the blood indexes predicting plaque characteristics. We investigated the relationship among soluble CD105, hypersensitive C-reactive protein (hs-CRP), and coronary plaque morphology.

METHODSA clinical study from April 2004 to December 2006 was conducted in 130 patients who were divided into 3 groups: 56 patients (43.1%) in stable angina (SA) group, 52 patients (40.0%) in unstable angina (UA) group and 22 patients (16.9%) in acute myocardial infarction group. The concentrations of soluble CD105 and hs-CRP were measured in all of the patients by cardioangiography (CAG). Plasma samples of arterial blood were collected prior to the procedure. The levels of soluble CD105 and hs-CRP were measured by enzyme-linked immunosorbent assay (ELISA).

RESULTSUnstable and ruptured plaque was found more frequently in patients with acute myocardial infarction and UA. External elastic membrane cross-sectional area (EEM CSA), plaque area, lipid pool area and plaque burden were significantly larger in the ruptured and unstable plaque group. Positive remodeling, thinner fabric-cap, smaller minimal lumen cross-sectional area (MLA), dissection and thrombus were significantly more frequent in the ruptured and unstable plaque group. Remodeling index (RI) was positively correlated with the levels of soluble CD105 in the UA group (r = 0.628, P < 0.01) and the acute myocardial infarction group (r = 0.639, P < 0.01). The levels of soluble CD105 and hs-CRP were higher in the ruptured plaque group. Soluble CD105 > 4.3 ng/ml was used to predict ruptured plaque with a receiver operating characteristic (ROC) curve area of 0.77 (95% confidence interval (CI), 66.8% - 87.2%), a sensitivity of 72.8%, a specificity of 78.0% and an accuracy of 70.2% (P < 0.01), similarly for hs-CRP > 5.0 mg/ml with a ROC curve area of 0.70 (95% CI, 59.2% - 80.2%), a sensitivity of 70.2%, a specificity of 76.2% and an accuracy of 67.2% (P < 0.01).

CONCLUSIONSThe plaque characteristics correlate with the clinical presentation. The elevation of soluble CD105 and hs-CRP is related to the plaque instability and rupture.

Aged ; Angina Pectoris ; blood ; pathology ; Antigens, CD ; blood ; C-Reactive Protein ; analysis ; Coronary Vessels ; diagnostic imaging ; pathology ; Endoglin ; Female ; Humans ; Male ; Middle Aged ; Myocardial Infarction ; blood ; pathology ; Receptors, Cell Surface ; blood ; Ultrasonography, Interventional ; methods

Interleukin (IL)-33 is an important mediator of innate immunity. Behcet's disease (BD) is an autoinflammatory disorder characterized by hyperactivity of the innate immune response. We measured serum levels of IL-33 and its receptor soluble ST2 (sST2) in patients with BD to investigate their association with disease activity. Serum levels of both IL-33 and sST2 were higher in patients with BD compared with those in normal controls (IL-33: 594.48+/-175.04 pg/mL in BD and 224.23+/-56.64 pg/mL in normal controls [P=0.048], sST2: 99.01+/-15.92 pg/mL in BD and 23.56+/-3.25 pg/mL in normal controls [P<0.001]). IL-33 and sST2 expression in skin tissue, as shown by immunohistochemistry, was higher in patients with BD compared with that in the normal controls. Serum sST2 level correlated significantly with the BD currently active form (BDCAF), Iranian BD dynamic activity measure (IBDDAM), erythrocyte sedimentation rate and C-reactive protein. Multiple linear regression showed that serum sST2 was an independent factor associated with IBBDAM (regression coefficient, 0.374; P=0.004), and BDCAF (regression coefficient, 0.236; P=0.047). These results demonstrate that IL-33 and sST2 are highly expressed in patients with BD and that serum sST2 is an independent factor associated with IBDDAM and BDCAF, suggesting a potential role for sST2 as a surrogate marker of disease activity in patients with BD.
Adult ; Behcet Syndrome/blood/*pathology ; Blood Sedimentation ; C-Reactive Protein/analysis ; Female ; Humans ; Immunohistochemistry ; Interleukins/*blood/metabolism ; Male ; Middle Aged ; Receptors, Cell Surface/*blood/metabolism ; Severity of Illness Index ; Skin/metabolism/pathology

PURPOSEMacrophages are known to be important for healing numerous injured tissues depending on their functional phenotypes in response to different stimuli. The objective of this study was to reveal macrophage phenotypic changes involved in exercise-induced skeletal muscle injury and regeneration.

METHODSAdult male Sprague-Dawley rats experienced one session of downhill running (16° decline, 16 m/min) for 90 min. After exercise the blood and soleus muscles were collected at 0 h, 6 h, 12 h, 1 d, 2 d, 3 d, 1 w and 2 w after exercise, separately.

RESULTSIt was showed that CD68 M1 macrophages mainly infiltrated into muscle necrotic sites at 1-3 d, while CD163 M2 macrophages were present in muscles from 0 h to 2 weeks after exercise. Using transmission electron microscopy, we observed activated satellite cells 1 d after exercise. Th1-associated transcripts of iNOS and Ccl2 were inhibited post exercise, while COX-2 mRNA was dramatically increased 12 h after running (p < 0.01). M2 phenotype marker Arg-1 increased 12 h and 3 d (p < 0.05, p < 0.01) after exercise, and Clec10a and Mrc2 were up-regulated in muscles 12 h following exercise (p < 0.05, p < 0.05).

CONCLUSIONThe data demonstrate the dynamic patterns of macrophage phenotype in skeletal muscle upon eccentric exercise stimuli, and M1 and M2 phenotypes perform different functions during exercise-induced skeletal muscle injury and recovery.

Animals ; Antigens, CD ; analysis ; Antigens, Differentiation, Myelomonocytic ; analysis ; Macrophages ; physiology ; Male ; Muscle, Skeletal ; injuries ; pathology ; Myoglobin ; blood ; Phenotype ; Physical Conditioning, Animal ; Rats ; Rats, Sprague-Dawley ; Receptors, Cell Surface ; analysis

The interleukin-33 (IL-33)/ST2 pathway has emerged as an intercellular signaling system that participates in antigen-allergen response, autoimmunity and fibrosis. It has been suggested that IL-33/ST2 signaling has been involved in the pathogenesis of rheumatoid arthritis (RA), because IL-33 and its receptor have been specifically mapped to RA synovium. The aim of this study was to determine the levels of IL-33 and sST2 in sera and synovial fluids in patients with RA. The serum level of IL-33 was significantly higher in patients with RA (294.9 +/- 464.0 pg/mL) than in healthy controls (96.0 +/- 236.9 pg/mL, P = 0.002). The synovial fluid level of IL-33 was significantly higher in RA patients than in osteoarthritis patients. The level of serum sST2 was higher in RA patients than in healthy controls (P = 0.042). A significant relationship was found between the levels of IL-33 and IL-1beta (r = 0.311, P = 0.005), and IL-33 and IL-6 (r = 0.264, P = 0.017) in 81 RA patients. The levels of IL-33, sST2 and C-reactive protein decreased after conventional disease-modifying antirheumatic drugs treatment in 10 patients with treatment-naive RA. Conclusively, IL-33 is involved in the pathogenesis of RA and may reflect the degree of inflammation in patients with RA.
Adult ; Aged ; Antirheumatic Agents/therapeutic use ; Arthritis, Rheumatoid/blood/drug therapy/*pathology ; C-Reactive Protein/analysis ; Female ; Humans ; Interleukin-1beta/analysis/blood ; Interleukin-6/analysis/blood ; Interleukins/*analysis/blood ; Male ; Middle Aged ; Osteoarthritis/blood/pathology ; Receptors, Cell Surface/*analysis/blood ; Synovial Fluid/metabolism

BACKGROUNDThe SLAM family recently has been reported to show an important biological role in lymphocyte development and immunological function, and it is efficient to highly purify hematopoietic stem cells using a simple combination of SLAM family members. To elucidate the presence of this family on acute lymphoblastic leukemia (ALL), as well as its relationship with the leukemia-initiating potential, we analyzed the expression pattern of this family members on human ALL progenitor cells, combined with serial xenotransplantation assay.

METHODSExpression analysis was carried out by flow cytometry. We combined the expression pattern of human CD(150), CD(244) and CD(48) with serial xenotransplantation of B-ALL progenitor cells to indicate their relationship.

RESULTSCD(48) and CD(244) were expressed on most B-ALL progenitor cells, the percentage being (93.08 ± 6.46)% and (63.37 ± 29.31)%, respectively. Interestingly, the proportion of CD(150)(+) cells declined obviously in engrafted cases ((24.94 ± 7.32)%) compared with non-engrafted cases ((77.54 ± 5.93)%, P < 0.01), which indicated that only blast cells with low percentage of CD(150)(+) population were able to reconstitute leukemia into primary, secondary and tertiary NOD/SCID mice.

CONCLUSIONSSLAM family members are present on B-ALL progenitor cells and the leukemia-initiating potential of leukemic blasts is correlated negatively with the proportion of CD(150)(+) cells, the percentage of which can serve as a useful predictor for engraftment success of B-ALL to immune deficient mice.

Adolescent ; Adult ; Aged ; Animals ; Antigens, CD ; analysis ; CD48 Antigen ; Child, Preschool ; Female ; Flow Cytometry ; Humans ; Infant ; Male ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Middle Aged ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; blood ; Receptors, Cell Surface ; analysis ; Receptors, Immunologic ; analysis ; Signaling Lymphocytic Activation Molecule Family ; Signaling Lymphocytic Activation Molecule Family Member 1 ; Transplantation, Heterologous

OBJECTIVETo investigate the association between hemoglobin scavenger receptor (CD163) expression levels on monocytic surfaces and coronary atherosclerotic severity in patients with coronary heart disease (CHD) as well as the roles of CD163 in inflammation and lipidperoxidation.

METHODSEighty-four patients were diagnosed as CHD according to the results of coronary angiography and ACC/AHA diagnostic criteria. The patients were divided into 3 groups: acute myocardial infarction (AMI) group (n = 30), unstable angina (UA) group (n = 30), stable angina (SA) group (n = 24). Another 20 patients with normal coronary artery served as control. Expression levels of CD163 on monocytes were detected by means of flow cytometry, and the results were shown as mean fluorescence intensity (mfi). All patients underwent coronary angiography and the results were further evaluated by Jenkins score. Serum CRP and LDL-C were also measured.

RESULTSThe expression levels of CD163 on monocytes in peripheral blood were significantly higher in CHD patients compared to controls (P < 0.01) in the order of AMI group [(84.4 +/- 6.9) mfi] > UA group [(64.1 +/- 5.5) mfi, P < 0.01 vs. AMI] > SA group [(46.7 +/- 6.5) mfi, P < 0.01 vs. AMI and UA] > control group [(22.0 +/- 6.1) mfi, P < 0.01 vs. AMI, UA and SA]. The expression levels of CD163 on monocytes in patients with CHD were positively correlated with Jenkins score (r = 0.9107, P < 0.01), CRP (r = 0.766, P < 0.01) and LDL-C (r = 0.749, P < 0.01).

CONCLUSIONSExpression levels of CD163 was significantly increased in patients with CHD and positively correlated with coronary heart disease severity and serum CRP and LDL-C.

Adult ; Aged ; Aged, 80 and over ; Antigens, CD ; metabolism ; Antigens, Differentiation, Myelomonocytic ; metabolism ; C-Reactive Protein ; analysis ; Cholesterol, LDL ; blood ; Coronary Disease ; metabolism ; pathology ; Female ; Humans ; Inflammation ; Lipid Peroxidation ; Male ; Middle Aged ; Receptors, Cell Surface ; metabolism ; Severity of Illness Index

OBJECTIVESTo observe the synthesis of Toll-like receptor (TLR) 4 protein and its mRNA expression in Kupffer cells (KCs) and evaluate the role of TLR 4 in liver injury to rats through alcohol-induced liver disease.

METHODSTwenty-eight Wistar rats were divided into two groups: ethanol-fed (group E) and control (group C). Group E rats were given ethanol at a dose of 5 - 12 g x kg(-1) x d(-1), while group C received dextrose. Animals from both groups were killed at 4 and 8 weeks. The KCs were isolated and synthesis of TLR 4 protein was determined by laser scanning confocal microscopy. TLR 4 mRNA expression in KCs was determined by reverse transcription polymerase chain reaction (RT-PCR) analysis. The levels of endotoxin, tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) in plasma were determined. Changes in liver pathology were observed.

RESULTSLaser scanning confocal microscopy showed that the intensity of fluorescence of TLR 4 protein in group E was stronger than group C. Ethanol administration led to a significant increase in TLR 4 mRNA expression in group E compared with group C (P < 0.05). The concentrations of plasma endotoxin, TNF-alpha and IL-6 were higher in group E than in group C (P < 0.05). Liver sections from rats in group E demonstrated marked pathological changes.

CONCLUSIONEthanol administration can lead to the synthesis of TLR 4 protein and its gene expression in KCs, indicating that TLR 4 may play a major role in the development of alcohol-induced liver injury.

Animals ; Drosophila Proteins ; Female ; Interleukin-6 ; blood ; Kupffer Cells ; physiology ; Lipopolysaccharide Receptors ; physiology ; Liver Diseases, Alcoholic ; etiology ; pathology ; Membrane Glycoproteins ; genetics ; physiology ; RNA, Messenger ; analysis ; Rats ; Rats, Wistar ; Receptors, Cell Surface ; genetics ; physiology ; Toll-Like Receptor 4 ; Toll-Like Receptors ; Tumor Necrosis Factor-alpha ; analysis