BACKGROUND: Leptin is a 16-KDa non-glycosylated peptide hormone synthesized almost exclusively by adipocytes. The well-known function of leptin is regulation of food intake and energy expenditure. Leptin also plays a regulatory role in immune and inflammatory process including cytokine production. The purpose of this study was to investigate the effect of leptin on the expression of several chemokine genes(RANTES, IL-8, MCP-1, IP-10, Mig, MIP-1alpha, MIP-1beta, and GRO-alpha) in THP-1 cells. MATERIALS AND METHODS: Total RNA of THP-1 cells were prepared by Trizol method, and then stimulated with the leptin(250 ng/microliter) or LPS(100 ng/microliter). We examined the expression patterns of various chemokine mRNAs in THP-1 cell lines by RT-PCR and Northern blot. RESULTS: Leptin did not induce the expression of chemokine mRNAs in THP-1 cells. The expression patterns of RANTES, IL-8, MCP-1, IP-10, and Mig mRNAs in THP-1 cells stimulated with leptin and LPS simultaneously was almost same to the patterns of LPS alone-induced chemokine mRNAs. RANTES mRNA expression was independent on the concentrations of leptin. Although leptin did not have strong effect on the expression of RANTES, IL-8, MCP-1, IP-10, Mig, MIP-1alpha, MIP-1beta, and GRO-alpha mRNAs in THP-1 cells, leptin could induce the expression of long isoform of leptin receptor(OB-RL) mRNA, and its expression was elevated in simultaneous stimulation of leptin and LPS. CONCLUSION: These data suggest that leptin is able to induce OB-RL in THP-1 cells, however, leptin has little effect on the expression of pro-inflammatory chemokine genes.
Adipocytes ; Blotting, Northern ; Cell Line ; Chemokine CCL3 ; Chemokine CCL4 ; Chemokine CCL5 ; Eating ; Energy Metabolism ; Interleukin-8 ; Leptin* ; RNA ; RNA, Messenger

BACKGROUND: Leptin is a 16-KDa non-glycosylated peptide hormone synthesized almost exclusively by adipocytes. The well-known function of leptin is regulation of food intake and energy expenditure. Leptin also plays a regulatory role in immune and inflammatory process including cytokine production. The purpose of this study was to investigate the effect of leptin on the expression of several chemokine genes(RANTES, IL-8, MCP-1, IP-10, Mig, MIP-1alpha, MIP-1beta, and GRO-alpha) in THP-1 cells. MATERIALS AND METHODS: Total RNA of THP-1 cells were prepared by Trizol method, and then stimulated with the leptin(250 ng/microliter) or LPS(100 ng/microliter). We examined the expression patterns of various chemokine mRNAs in THP-1 cell lines by RT-PCR and Northern blot. RESULTS: Leptin did not induce the expression of chemokine mRNAs in THP-1 cells. The expression patterns of RANTES, IL-8, MCP-1, IP-10, and Mig mRNAs in THP-1 cells stimulated with leptin and LPS simultaneously was almost same to the patterns of LPS alone-induced chemokine mRNAs. RANTES mRNA expression was independent on the concentrations of leptin. Although leptin did not have strong effect on the expression of RANTES, IL-8, MCP-1, IP-10, Mig, MIP-1alpha, MIP-1beta, and GRO-alpha mRNAs in THP-1 cells, leptin could induce the expression of long isoform of leptin receptor(OB-RL) mRNA, and its expression was elevated in simultaneous stimulation of leptin and LPS. CONCLUSION: These data suggest that leptin is able to induce OB-RL in THP-1 cells, however, leptin has little effect on the expression of pro-inflammatory chemokine genes.
Adipocytes ; Blotting, Northern ; Cell Line ; Chemokine CCL3 ; Chemokine CCL4 ; Chemokine CCL5 ; Eating ; Energy Metabolism ; Interleukin-8 ; Leptin* ; RNA ; RNA, Messenger

BACKGROUND AND OBJECTIVES: The number of eosinophil in nasal polyps has been reported to be strongly elevated when compared to non-affected nasal tissue, indicating an important role for eosinophils in the pathogenesis of nasal polyposis. The mechanisms determining selective eosinophilic tissue infiltration into diseased nasal mucosa as yet are specualtive. Panleukotactic factors also known to be present on nasal polyps cannot explain the type-selective tissue infiltration in eosinophilic or neutrophilic-featured diseases. Chemokines are known to have leukocyte subtype-selective chemotactic properties in vitro and thus are candidates explaining leukocytic characteristic tissue infiltration. The aim of this study was to investigate whether specific chemokines are associated with different forms of nasal polyps. This study was designed to demonstrate the expressions of various CC chemokines. MATERIALS AND METHODS: Nasal polyp from patients with systemic allergy (AP group, n=7) and negative allergic skin tests (NP group, n=10) were sampled. Expressions of RANTES, eotaxin, MCP-1, MIP-1alpha,beta were studies by RT-PCR and immunohistochemical studies. RESULTS: Expression and mean density of RANTES, MCP-1, MIP-1beta were significantly stronger in NP group than in AP group (p<0.05). However, those of eotaxin and MIP-1alpha were significantly stronger in AP group than in NP group (p<0.01). CONCLUSION: This results suggest that only selective chemokines could be involved to develop the pathologic conditions in different type of nasal polyp.
Chemokine CCL3 ; Chemokine CCL4 ; Chemokine CCL5 ; Chemokines ; Chemokines, CC* ; Eosinophils ; Humans ; Hypersensitivity ; Leukocytes ; Nasal Mucosa ; Nasal Polyps* ; Skin Tests

BACKGROUND AND OBJECTIVES: The cause of nasal polyp is unsure but inflammation is thought to be an important factor in the development of nasal poyps. CC chemokine is a powerful chemotactic cytokine for inflammatory cells. We designed this study to investigate whether specific CC chemokines are associated with different forms of nasal polyps and their changes according to antibiotic treatment. MATERIALS AND METHODS: Nasal polyp from patients with atopy (AP group, n=12) and without atopy (NP group, n=20) were sampled. Expressions of RANTES, eotaxin, MCP-2, MCP-3 and MIP-1alpha were studied by an immunohistochemical study. Specimens of non-allergic nasal turbinates were used as the control group from 14 patients who were operated for nasal blockage. All patients were divided into 2 groups. One group was treated with antibiotics for 10 days before operation. The other was non-treated. RESULTS: Between the NP and AP group, the ratio of stained cells except anti-MCP 2 monoclonal antibody in the AP group was more increased than that of the NP group. Among them, RANTES and eotaxin were increased significantly (p<0.05). There was a significant difference of the expression of 5 CC chemokines between the treated and non-treated groups (p<0.05). CONCLUSIONS: These results suggest that chemokines play an important role in the development of nasal polyps, and different kinds of chemokines can be involved according to the cause of nasal polyps and CC chemokines affected by antibiotic treatment.
Anti-Bacterial Agents ; Chemokine CCL3 ; Chemokine CCL5 ; Chemokines ; Chemokines, CC ; Humans ; Inflammation ; Nasal Obstruction ; Nasal Polyps* ; Turbinates

BACKGROUND AND OBJECTIVES: The cause of nasal polyp is unsure but inflammation is thought to be an important factor in the development of nasal poyps. CC chemokine is a powerful chemotactic cytokine for inflammatory cells. We designed this study to investigate whether specific CC chemokines are associated with different forms of nasal polyps and their changes according to antibiotic treatment. MATERIALS AND METHODS: Nasal polyp from patients with atopy (AP group, n=12) and without atopy (NP group, n=20) were sampled. Expressions of RANTES, eotaxin, MCP-2, MCP-3 and MIP-1alpha were studied by an immunohistochemical study. Specimens of non-allergic nasal turbinates were used as the control group from 14 patients who were operated for nasal blockage. All patients were divided into 2 groups. One group was treated with antibiotics for 10 days before operation. The other was non-treated. RESULTS: Between the NP and AP group, the ratio of stained cells except anti-MCP 2 monoclonal antibody in the AP group was more increased than that of the NP group. Among them, RANTES and eotaxin were increased significantly (p<0.05). There was a significant difference of the expression of 5 CC chemokines between the treated and non-treated groups (p<0.05). CONCLUSIONS: These results suggest that chemokines play an important role in the development of nasal polyps, and different kinds of chemokines can be involved according to the cause of nasal polyps and CC chemokines affected by antibiotic treatment.
Anti-Bacterial Agents ; Chemokine CCL3 ; Chemokine CCL5 ; Chemokines ; Chemokines, CC ; Humans ; Inflammation ; Nasal Obstruction ; Nasal Polyps* ; Turbinates

PURPOSE: Portal vein transfusion (PVT) has been known to induce immunosuppression or tolerance and Kupffer cell was identified to play an important role in the phenomenon. The purposes of this study were investigating PVT effect on gene regulation in Kupffer cells and subsequent change in serum cytokine. METHODS: For investigating the effect of PVT, Kupffer cells were isolated from the mice (BalbC) of six groups; 1 hour sham operation (S), 1 hour portal vein saline injection (PVS), 1 hour PVT, 24 hour S, 24 hour PVS, and 24 hour PVT groups. Each group was composed of 3 mice. Total RNAs isolated from Kupffer cells were subjected to RT-PCR differential display. The bands of 24 hour group showing increased expression was cloned for the sequencing analysis. RESULTS: Macrophage inflammatory protein 1 alpha (MIP-1alpha) was identified from the bands of increased expression. In PVT groups, increased expression of MIP-1alpha mRNA in Kupffer cells coincided with elevated serum level of MIP-1alpha. CONCLUSION: MIP-1alpha may be one of the important cytokines involved in PVT induced immunosuppression or tolerance.
Animals ; Chemokine CCL3* ; Clone Cells ; Cytokines ; Immunosuppression ; Kupffer Cells* ; Mice ; Portal Vein* ; RNA ; RNA, Messenger*

BACKGROUND: We tested the hypothesis that dengue haemorrhagic fever (DHF) is associated with a T(H)1-skewed immune response as opposed to dengue fever (DF). METHODS: We estimated intracellular (in T-cells) and serum levels of designate T(H)1/T(H)2 cytokines [interferon-gamma (IFN-gamma), interleukin-4 (IL-4), and tumor necrosis factor-alpha] and macrophage inflammatory protein-1alpha (MIP-1alpha) at admission, 48 h, and day 5 in 20 adults with dengue (DF=10, DHF=10) and 10 dengue-naive healthy controls. RESULTS: At admission, intracellular IFN-gamma/IL-4 ratio in CD4+ T-cells and proportion of MIP-1alpha-positive CD8+ T-cells were significantly higher in patients with DHF [7.21 (5.36~10.81) vs. 3.04 (1.75~4.02); p=0.011 and 6.2% (3.2~8.2%) vs. 2.4% (2.0~3.6%); p=0.023]. The latter showed a significant positive correlation with IFN-gamma/IL-4 ratio in CD4+ T-cells (Spearman's rho=0.64; p=0.003), percentage-change in haematocrit (rho=0.47; p=0.048), and serum alanine aminotransferase level (rho=0.61; p=0.009). CONCLUSION: We conclude that DHF is associated with a T(H)1-skewed immune response. Further, MIP-1alpha in CD8+ T-cells is an important immunologic correlate of disease severity in dengue.
Adult ; Alanine Transaminase ; Chemokine CCL3 ; Cytokines ; Dengue ; Fever ; Humans ; Interferon-gamma ; Interleukin-4 ; Macrophages ; Necrosis ; T-Lymphocytes

OBJECTIVETo observe changes in the concentrations of MIP-1alpha and TNF-alpha and their influence on sperm in the seminal plasma of infertile males.

METHODSWe measured the concentrations of MIP-1alpha and TNF-alpha in the seminal plasma of 110 infertile patients and 30 normal fertile men by ELISA and radioimmunoassay, and compared them with sperm concentration, sperm viability, sperm motility, leukocytospermia and serum anti-sperm antibodies (AsAb).

RESULTSThe infertility group, particularly the oligospermia cases, showed significantly higher concentrations of MIP-1alpha and TNF-alpha in the seminal plasma ([179.45 +/- 24.54] pg/ml and [4.66 +/- 2.01] ng/ml) than the normal fertile men ([89.64 +/- 13.27] pg/ml and [2.90 +/- 1.23] ng/ml) (P < 0.01). In comparison, the concentrations of MIP-1alpha and TNF-alpha were (196.04 +/- 23.54) pg/ml and (5.31 +/- 2.47) ng/ml versus (154.22 +/- 26.38) pg/ml and (3.94 +/- 2.09) ng/ml in the poor and normal sperm viability groups (P < 0.05 or P < 0.01), (210.39 +/- 21.43) pg/ml and (5.14 +/- 2.61) ng/ml versus (139.87 +/- 27.62) pg/ml and (4.11 +/- 2.26) ng/ml in the low and normal sperm motility groups (P < 0.05 or P < 0.01), (203.14 +/- 24.65) pg/ml and (5.28 +/- 2.66) ng/ml versus (155.76 +/- 21.42) pg/ml and (4.04 +/- 2.24) ng/ml in the leukocytospermia and non-leukocytospermia groups (P < 0.05 or P < 0.01), and (234.05 +/- 27.60) pg/ml and (5.63 +/- 2.31) ng/ml versus (124.85 +/- 23.56) pg/ml and (3.69 +/- 2.15) ng/ml in the serum AsAb positive and negative groups (P < 0.05 or P < 0.01), most significantly increased in the serum AsAb positive group.

CONCLUSIONThe concentrations of MIP-1alpha and TNF-alpha in the seminal plasma are closely related with sperm count and function, and their detection helps to assess the severity of male infertility and improve its clinical treatment.

Adult ; Case-Control Studies ; Chemokine CCL3 ; analysis ; Humans ; Infertility, Male ; blood ; physiopathology ; Male ; Semen ; chemistry ; Tumor Necrosis Factor-alpha ; analysis

OBJECTIVETo observe the in vivo antitumor activity of murine liver tumor vaccine expressing MIP-1alpha mediated by recombinant adenoviral vector.

METHODSThe infection efficacy was measured by GFP expression 48 hours after infection of Hepa1-6, and the number of cells was counted daily for 14 days. 5 x 10(6) modified Hepa1-6 cells were inoculated subcutaneously to C57BL/6 mice and the tumor-free animals were rechallenged by 2 x 10(6) wild-type Hepa1-6 cells or syngenic EL4 cells four weeks later. The tumor volume was measured twice a week.

RESULTSAdenoviral vectors could efficiently infect Hepa1-6 cells in vitro, and the in vitro growth rate of AdmMIP-1alpha modified Hepa1-6 cells was not affected; however the in vivo tumorigenicity was significantly decreased, compared with that of control vector modified Hepa1-6. Rechallenge of the tumor-free mice four weeks after administration of AdmMIP-1alpha with the parental Hepa1-6 cells resulted in significant inhibition of tumor growth, but there was no significant difference when rechallenged with EL4.

CONCLUSIONSThe liver cancer cells expressing mMIP-1alpha mediated by recombinant adenoviral vector decrease tumorigenicity and elicit specific immunological protection, and could be used as an effective liver tumor vaccine.

Adenoviridae ; genetics ; Animals ; Cancer Vaccines ; immunology ; Chemokine CCL3 ; Chemokine CCL4 ; Genetic Therapy ; Liver Neoplasms, Experimental ; therapy ; Macrophage Inflammatory Proteins ; genetics ; Mice ; Mice, Inbred C57BL ; Vaccines, Synthetic ; immunology

UNLABELLEDBACKGROWND: Macrophage inflammatory protein-1α (MIP-l α/CCL3) belongs to the C-C chemokine family (CCL3), which can be secreted by macrophages, other types of hematopoietic cells and bone marrow stromal cells. Higher levels of MIP-1α were found to be associated with several kinds of hematologic malignancies, including multiple myeloma (MM), chronic lymphocytic leukemia (CLL) and chronic myeloid leukemia (CML). Moreover, MIP-1α has been reported to be an adverse prognostic factor for CLL. However, the impact of MIP-1α on acute myeloid leukemia (AML) has been poorly investigated.

OBJECTIVETo investigate the influence of MIP-1α on proliferction of AML cells.

METHODSUsing MLL-AF9 induced AML mouse model, the expression of MIP-1α was measured by real time quantitative RT-PCR. AML cell proliferation was examined by cell counting and colony forming assay (CFC). The influence of blocking the MIP-1α action on the growth and pathogenic ability of AML cells was explored by using the small molecule antagonist for interfering interaction of MIP-1α with its receptor CCR1.

RESULTSThe MIP-1α could promote the proliferation and colony formation of AML cells, the blocking MIP-1a could inhibit the growth of AML cells and delay onset of AML.

CONCLUSIONThe MIP-1a promotes the occurence and progression of AML, therefore blocking the MIP-1α signal pathway may be served as a strategy to inhibit the growth of AML cells, and MIP-1α can be a potential target for treatment of AML.

Animals ; Cell Line, Tumor ; Cell Proliferation ; Chemokine CCL3 ; Chemokine CCL4 ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; Leukemia, Myeloid, Acute ; Macrophage Inflammatory Proteins ; Mice ; Multiple Myeloma ; Receptors, CCR1