BACKGROUNDScavenger receptor that binds phosphatidylserine and oxidized lipoprotein/CXC chemokine ligand 16 (SR-PSOX/CXCL16) promotes foam cell formation through the tumor necrosis factor (TNF)-alpha mediated mechanism. Because chemokine CXCL16 could be expressed in atherosclerotic lesions and induce smooth muscle cell (SMC) proliferation, we presume that the monocyte SR-PSOX/CXCL16 detection in the patients' peripheral blood will be important for early diagnosis and prognosis of atherosclerosis (AS).

METHODSEnrolled in this study were 40 patients with acute coronary syndrome (ACS), including 20 patients with acute myocardial infarction (AMI) and 20 patients with unstable angina pectoris (UAP), and 20 normal controls. Monocytes in the peripheral blood were isolated, and the changes of expression of CXCL16/SR-PSOX mRNA were compared using reverse transcription-polymerase chain reaction (RT-PCR), with beta-actin as internal control. We compared the expression of CXCL16/SR-PSOX in the ACS subgroups, using Western-blot to analyze protein expression levels. Tissue sections were made from biopsy specimens taken from patients with infective endocarditis, liver cirrhosis, and lung cancer as well as normal controls. And the expression of CXCL16/SR-PSOX was analyzed with a confocal microscope.

RESULTSThe expression of CXCL16/SR-PSOX mRNA and protein in the monocytes of peripheral blood was significantly higher in ACS patients than in normal controls (P < 0.05); however, there was no significant difference in CXCL16/SR-PSOX expression between UAP group and AMI group (P > 0.05). Immunofluorescence showed that there were low expression of SR-PSOX in normal vascular endothelial cells and enhanced expression in every layer of the infected vessels, while spreading from endothelial cells to surrounding tissues as infection worsens. Confocal microscopy showed that the expression of SR-PSOX was enhanced in the infiltrated lymphocytes in liver cirrhosis, and that the expression level was proportionate to the degree of inflammation in the portal hepatis and folia.

CONCLUSIONSThe expression of CXCL16/SR-PSOX in the monocytes of peripheral blood was significantly higher in ACS patients than in the controls. CXCL16/SR-PSOX-mediated inflammation may contribute to the pathogenesis of ACS, and CXCL16 may play an important role in the pathogenesis and development of AS in humans.

Acute Coronary Syndrome ; immunology ; Blotting, Western ; Chemokine CXCL16 ; Chemokines, CXC ; blood ; genetics ; Coronary Angiography ; Fluorescent Antibody Technique ; Humans ; RNA, Messenger ; blood ; Receptors, Scavenger ; blood ; genetics

OBJECTIVEThis study examined the expressions of plasma stromal cell derived factor-1 (SDF-1) and CXCR4 mRNA in peripheral blood mononuclear cells (PBMC) of children with Kawasaki disease (KD) and aimed to explore the significance of SDF-1 and CXCR4 mRNA in KD.

METHODSFifty-six children with KD (12 cases complicated by coronary artery lesions) and 60 age and gender-matched healthy children (normal controls) were enrolled in this study. Plasma SDF-1 levels and CXCR4 mRNA expression in PBMC were measured using ELISA and real-time quantitative PCR at the acute and convalescence stages of KD.

RESULTSPlasma SDF-1 levels (1833 +/- 395 ng/L vs 1126 +/- 408 ng/L; P < 0.05) and the CXCR4 mRNA expression in PBMC (6.57 +/- 2.81 vs 2.58 +/- 1.01; P < 0.01) in KD patients were significantly higher than those in normal controls at the acute stage. Both plasma SDF-1 levels and CXCR4 mRNA expression in KD patients decreased significantly at the convalescence stage, but nevertheless remained higher than those in the normal controls. The patients with concomitant coronary artery lesions showed higher CXCR4 mRNA levels than without at the acute stage (8.19 +/- 2.39 vs 6.13 +/- 2.77; P < 0.05).

CONCLUSIONSPlasma SDF-1 concentration and CXCR4 mRNA expression in PBMC increased in KD patients. CXCR4 mRNA might be involved in the development of coronary artery lesions in KD.

Chemokine CXCL12 ; Chemokines, CXC ; blood ; Child, Preschool ; Female ; Humans ; Infant ; Leukocytes, Mononuclear ; metabolism ; Male ; Mucocutaneous Lymph Node Syndrome ; blood ; RNA, Messenger ; blood ; Receptors, CXCR4 ; genetics

BACKGROUNDThe immunological differences between children and adults with AIDS in China are not well documented. Th1/Th2 cytokines and chemokines are two types of immune factors intimately involved in disease progression of HIV-1 infection. This study aimed to identify changes in plasma levels of Th1/Th2 cytokines inerleukin (IL)-18, IL-16, IL-10 and chemokines regulated on activation, normal T cell expressed and secreted (RANTES), stromal cell-derived factor-1 (SDF-1) and monocyte chemoattractant protein-1 (MCP-1) in HIV-1-infected children and adults in China.

METHODSSeventy-five children with AIDS and 35 adult AIDS patients were recruited and clinical data were collected. CD4(+) T lymphocyte counts were measured by flow cytometery and plasma HIV RNA levels were measured by quantitative RT-PCR. Plasma levels of IL-18, IL-10, IL-16, RANTES, MCP-1, SDF-1alpha and SDF-1beta were quantified by enzyme-linked immunosorbent assay. The levels of beta2-microglobulin (beta2-MG) and soluble Fas (sFas) were measured to validate the level of humoral and cellular immune activation.

RESULTSThe mean levels of all cytokines in pediatric and adult AIDS patients were significantly higher than in their healthy controls (P < 0.01). The mean levels of these cytokines were higher in pediatric patients than in adult patients (P < 0.05, except for SDF-1alpha and beta2-MG). Some of the cytokine levels in patients younger than 6 years old was higher than in older children and adults with AIDS (IL-10, IL-18, SDF-1alpha, MCP, RANTES and sFas, P < 0.05). Levels of IL-18, IL-10, RANTES and beta2-MG of pediatric patients increased as the levels of viral load increased (P < 0.05).

CONCLUSIONSAbnormal immune activation can be measured in Chinese pediatric and adult patients with AIDS, and is higher in children than in adult patients. The cytokines levels coincide with disease progression of AIDS, but have no direct relationship with total CD4(+) T cell count.

Acquired Immunodeficiency Syndrome ; blood ; virology ; Adult ; Age Distribution ; Aged ; Chemokine CCL2 ; blood ; Chemokine CCL5 ; blood ; Chemokine CXCL12 ; blood ; Chemokines ; blood ; Child ; Child, Preschool ; Enzyme-Linked Immunosorbent Assay ; Female ; Flow Cytometry ; HIV-1 ; genetics ; Humans ; Interleukin-10 ; blood ; Interleukin-16 ; blood ; Interleukin-18 ; blood ; Interleukins ; blood ; Male ; Middle Aged ; RNA, Viral ; genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Viral Load

OBJECTIVETo study in the linkage between eotaxin-3 gene polymorphisms and allergic asthma susceptivity, blood plasma IgE or peripheral blood eosinophil in adult population of Han nationality from Hubei province of China.

METHODSPolymerase chain reaction (PCR), single strand conformation polymorphism (SSCP), tetra-primer PCR technique and restriction analysis were applied to identify the single nucleotide polymorphism.

RESULTSThe allele frequency of eotaxin-3 +2497 G, total levels of plasma IgE and peripheral blood eosinophil counts revealed the significant difference between control and allergic asthma group, that the P value was 0.011, 0.021 or 0.029 respectively. The allele frequency of eotaxin-3 +77 T and total levels of plasma IgE showed to have no significant difference between control and allergic asthma group, that the P value was 0.824 and 0.473 respectively. However, the peripheral blood eosinophil counts was significantly different between control and allergic asthma group, and the P value was 0.044.

CONCLUSIONSingle nucleotide polymorphism of eotaxin-3 +2497 is associated with the asthma susceptibility, peripheral eosinophil counts and total levels of plasma IgE in adult population from Hubei province, and polymorphism of +77 is associated with peripheral eosinophil counts.

Adult ; Alleles ; Asthma ; genetics ; immunology ; Base Sequence ; Chemokine CCL26 ; Chemokines, CC ; genetics ; China ; ethnology ; DNA Mutational Analysis ; Female ; Genetic Predisposition to Disease ; Humans ; Immunoglobulin E ; blood ; Male ; Middle Aged ; Molecular Sequence Data ; Polymorphism, Genetic ; Young Adult

We investigated whether the production and gene expression of Gro-alpha and RANTES in Kawasaki disease differ in measles. Forty-two samples from 14 patients in different clinical stages of Kawasaki disease, eight samples from 8 patients in the acute stage of measles and seven samples from 7 healthy children were collected. The present study was performed using ELISA and RT-PCR for the productions and gene expression of the chemokines. The production of Gro-alpha was markedly elevated during the acute stage of measles compared with Kawasaki disease. Moreover, the expression of Gro-alpha was increased in every case of measles, but not in Kawasaki disease. The production of RANTES was elevated in the acute stage of both diseases when compared to the healthy control. However, the plasma RANTES level did not change significantly according to the clinical stages of Kawasaki disease. A correlation between the production and gene expression of RANTES and Gro-alpha was not found in Kawasaki disease. These results suggest that Kawasaki disease differs from measles with regard to Gro-alpha production and expression, but not RANTES. Gro-alpha might play an important role in the acute stage of measles, however not in Kawasaki disease. Further studies are needed to clarify the efficacy of Gro-alpha as a marker in measles.
Biological Markers ; Chemokines/blood/*genetics ; Chemotactic Factors/blood/*genetics ; Child ; Child, Preschool ; Comparative Study ; Female ; Gene Expression/immunology ; Human ; Infant ; Intercellular Signaling Peptides and Proteins/blood/*genetics ; Leukocytes, Mononuclear/*physiology ; Male ; Measles/*immunology/physiopathology ; Mucocutaneous Lymph Node Syndrome/*immunology/physiopathology ; RANTES/blood/*genetics ; RNA, Messenger/analysis

OBJECTIVETo investigate whether emodin exerts protective effects on mouse with allergic asthma.

METHODSA mouse model of allergic airway inflflammation was employed. The C57BL/6 mice sensitized and challenged with ovalbumin (OVA) were intraperitoneally administered 10 or 20 mg/kg emodin for 3 days during OVA challenge. Animals were sacrificed 48 h after the last challenge. Inflammatory cell count in the bronchoalveolar lavage fluid (BALF) was measured. The levels of interleukin (IL)-4, IL-5, IL-13 and eotaxin in BALF and level of immunoglobulin E (IgE) in serum were measured with enzyme-linked immuno sorbent assay kits. The mRNA expressions of IL-4, IL-5, heme oxygenase (HO)-1 and matrix metalloproteinase-9 (MMP-9) were determined by real-time quantitative polymerase chain reaction.

RESULTSEmodin induced significant suppression of the number of OVA-induced total inflammatory cells in BALF. Treatment with emodin led to significant decreases in the levels of IL-4, IL-5, IL-13 and eotaxin in BALF and total IgE level in serum. Histological examination of lung tissue revealed marked attenuation of allergen-induced lung eosinophilic inflammation. Additionally, emodin suppressed IL-4, IL-5 and MMP-9 mRNA expressions and induced HO-1 mRNA expression.

CONCLUSIONEmodin exhibits anti-inflammatory activity in the airway inflammation mouse model, supporting its therapeutic potential for the treatment of allergic bronchial asthma.

Animals ; Bronchoalveolar Lavage Fluid ; cytology ; Chemokines ; metabolism ; Disease Models, Animal ; Emodin ; chemistry ; pharmacology ; therapeutic use ; Female ; Gene Expression Regulation ; drug effects ; Heme Oxygenase-1 ; genetics ; metabolism ; Immunoglobulin E ; blood ; Interleukins ; genetics ; metabolism ; Leukocytes ; drug effects ; metabolism ; Lung ; drug effects ; metabolism ; pathology ; Matrix Metalloproteinase 9 ; genetics ; metabolism ; Mice, Inbred C57BL ; Ovalbumin ; Pneumonia ; blood ; drug therapy ; pathology ; Protective Agents ; pharmacology ; therapeutic use ; RNA, Messenger ; genetics ; metabolism

OBJECTIVETo observe induction of heat shock reaction by pretreatment of Doxorubicin (DXR) in long-term cold preservation-reperfusion injury of the rat liver.

METHODSThe rats were administered intravenously by DXR at a dose of 1 mg/kg body weight in DXR group and by saline in control group. After 48 hours, the rat liver was perfused by using cold University of Wisconsin (UW) solutions and was preserved in UW solution at 4 degrees C for 48 hours. Recipient liver was perfused for 1 and 3 hours after orthotopic liver transplantation. Tumor necrosis factor-alpha (TNF-alpha) mRNA, cytokine-induced neutrophil chemoattractant (CINC) mRNA, macrophage inflammatory protein (MIP-2) mRNA was measured by RT-PCR and heat shock protein 72 (HSP72), nuclear factor-kappaB (NF-kappaB) by Western blot. The serum levels of TNF-alpha, CINC, MIP-2 by ELISA and AST were measured. The survival rate of 7 days was observed.

RESULTSThe expression of TNF-alpha mRNA, CINC mRNA and MIP-2 mRNA was stronger in control group than in DXR group. HSP72 was expressed in SA group but not in control group and oppositely NF-kappaB was expressed in control group but not in DXR group. Serum AST, TNF-alpha, CINC and MIP-2 concentrations were significantly lower in DXR group than in control group (P < 0.05). The survival rate of 7 days was significantly higher in DXR group than in control group (50% vs. 0%, P < 0.05).

CONCLUSIONSThese data suggested that long-term cold ischemia-reperfusion injury was attenuated in liver graft with pretreatment of DXR. The induction of HSP72 may offer protection to hepatocytes by restraining the activation of NF-kappaB and inflammation.

Animals ; Chemokines, CXC ; biosynthesis ; genetics ; Cryopreservation ; Doxorubicin ; pharmacology ; HSP72 Heat-Shock Proteins ; biosynthesis ; Liver ; blood supply ; drug effects ; metabolism ; Liver Transplantation ; Male ; RNA, Messenger ; genetics ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; etiology ; prevention & control ; Reverse Transcriptase Polymerase Chain Reaction ; Tissue Survival ; Tumor Necrosis Factor-alpha ; biosynthesis ; genetics

PURPOSE: Rheumatoid arthritis (RA) is an inflammatory joint disorder, the progression of which leads to the destruction of cartilage and bone. Chemokines are involved in RA pathogenesis. In this study, we investigated the chemokine signaling pathway associated with CCL2 in peripheral blood (PB) and synovial tissues (ST) of RA patients based on our previous work about chemokine signaling pathway involved in the activation of CCL2 production in collagen-induced arthritis rat ST. MATERIALS AND METHODS: Total RNA was isolated from PB leukocytes and synovium of the knee joint in both RA patients and control populations. Real-time polymerase chain reaction was used to determine CCL4, CCR5, c-Jun, c-Fos, and CCL2 expressions. Serum level of CCL2 was assessed by enzyme-linked immunosorbent assay, and the production of CCL2 in ST was analyzed immunohistochemically. RESULTS: The expressions of CCL4, CCR5, c-Jun, c-Fos, and CCL2 messenger RNA in RA patients were significantly higher than those in healthy controls, both in ST and on PB leukocyte. Serum CCL2 levels were elevated in RA patients. Histological examination of rheumatoid joints revealed extensive CCL2 expression in RA ST. CONCLUSION: CCL2, CCL4, c-Jun, c-Fos, and CCR5 may play an important role in the recruitment of PB leukocytes into the RA joints. These data provide evidence that the chemokine signaling pathway is involved in CCL2 expression in RA patient tissues, which may contribute to chronic inflammation associated with RA. Targeting this signaling pathway may provide a novel therapeutic avenue in RA.
Adult ; Animals ; Arthritis, Rheumatoid/*blood/metabolism ; Case-Control Studies ; Chemokine CCL2/*blood/metabolism ; Chemokines/metabolism ; Enzyme-Linked Immunosorbent Assay ; Female ; Gene Expression ; Humans ; Male ; Middle Aged ; RNA, Messenger/genetics/metabolism ; Rats ; Real-Time Polymerase Chain Reaction ; Signal Transduction ; Synovial Membrane/*metabolism

Animals ; Arterioles ; metabolism ; pathology ; Blood Pressure ; drug effects ; Chemokine CX3CL1 ; Chemokines, CX3C ; analysis ; genetics ; Chronic Disease ; Flavonoids ; pharmacology ; Hypertension, Pulmonary ; prevention & control ; Hypertrophy, Right Ventricular ; prevention & control ; Hypoxia ; complications ; metabolism ; Lung ; metabolism ; Male ; Membrane Proteins ; analysis ; genetics ; Pulmonary Artery ; metabolism ; pathology ; RNA, Messenger ; analysis ; Rats ; Rats, Sprague-Dawley