1.Expressions of MIP-1alpha, MCP-1 and their receptors CCR-1, CCR-2 in chronic myeloid leukemia cells.
Wei-Liang WANG ; Ti SHEN ; Yu-Rong HUI ; Xi-Chun GU ; Rong-Sheng LI
Journal of Experimental Hematology 2006;14(3):433-436
This study was aimed to explore the expression of MIP-1alpha, MCP-1 and their receptors CCR-1, CCR-2 in bcr/abl fusion gene positive CML cells, and to study the effects of P210(bcr/abl) fusion protein tyrosine kinase on expression of MIP-1alpha, MCP-1 and their receptors CCR-1, CCR-2 mRNAs in chronic myeloid leukemia cells. The expression levels of MIP-1alpha, MCP-1 and their receptors CCR-1, CCR-2 mRNA were detected by semi-quantitative RT-PCR in bcr/abl negative cells, bcr/abl positive cells, and P210(bcr/abl)-Rb-C-Box positive cells. The results showed that MIP-1alpha and CCR-1 mRNAs were expressed in bcr/abl negative cells, but not in positive cells. Both MCP-1 and CCR-2 mRNA cannot be detected in both bcr/abl positive and negative cells. After inhibiting P210(bcr/abl) tyrosine kinase activity by Rb-C-Box, expressions of MIP-1alpha and CCR-1 mRNAs were restored to normal (similar to P210(bcr/abl) negative cells). It is concluded that P210(bcr/abl) fusion protein inhibits the expression of MIP-1alpha and CCR-1 in chronic myeloid leukemia cells, but does not inhibit MCP-1 and CCR-2 mRNA expressions in these leukemia cells.
Chemokine CCL2
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biosynthesis
;
genetics
;
Chemokine CCL3
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Chemokine CCL4
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Humans
;
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
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metabolism
;
Macrophage Inflammatory Proteins
;
biosynthesis
;
genetics
;
Receptors, CCR1
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Receptors, CCR2
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Receptors, Chemokine
;
biosynthesis
;
genetics
;
Tumor Cells, Cultured
2.Microvessel counts and the expressions of chemotactic factors in the pathological scar tissues.
Li QIAN ; Bai-Cheng ZHAO ; Li PI ; Qing LU
Journal of Central South University(Medical Sciences) 2005;30(3):340-348
OBJECTIVE:
To explore the microvessel counts and the expressions of interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1), and macrophage inflammatory protein-1 ( MIP-1) alpha mRNA in the pathological scar tissues.
METHODS:
Immunohistochemical method of avidin-biotin complex was used for microvessel counts on the routinely formalin-fixed and paraffin-embedded sections of specimens of hypertrophic scars, keloids, normal skin, and surgical scar, and in situ hybridization for the expressions of IL-8, MCP-1, MIP-1alpha mRNA.
RESULTS:
The microvessel counts as well as the positive rates and the scorings of IL-8, MCP-1, and MIP-1alpha mRNA were significantly higher in pathological scars than those in the normal skin and surgical scar (all P < 0.05). The microvessel counts were significantly higher in the positive cases of IL-8, MCP-1 and MIP-1alpha mRNA than those in the negative ones (P < 0.05). The close positive correlations were found among the microvessel counts and the expressive scorings of 3 factors (P < 0.05). The close positive correlations were also found among the expressive scorings of IL-8, MCP-1, and MIP-1alpha mRNA in pathological scars. Microvessel counts were significantly higher in hypertrophic scars with the course less than 1 year than those with the course more than 1 year.
CONCLUSION
IL-8, MCP-1 and MIP-1alpha play important roles in promoting the neovascularization of pathological scars.
Adolescent
;
Adult
;
Burns
;
complications
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Capillaries
;
metabolism
;
Chemokine CCL2
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biosynthesis
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genetics
;
Chemokine CCL3
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Chemokine CCL4
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Cicatrix
;
etiology
;
metabolism
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Female
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Humans
;
Interleukin-8
;
biosynthesis
;
genetics
;
Macrophage Inflammatory Proteins
;
biosynthesis
;
genetics
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Male
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Middle Aged
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RNA, Messenger
;
biosynthesis
;
genetics
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Skin
;
blood supply
3.Effect of macrophage inflammatory protein-1alpha and its mRNA on airway inflammation of mouse asthma model.
Chang-chong LI ; Wei-xi ZHANG ; Xiao-fang CHEN ; Li-wei XIE ; Qiu-sha HE ; Xiao-guang HU ; Jian LIN ; Meng-rong LI ; Rong-xi WU ; Zheng-xia ZHANG
Chinese Journal of Pediatrics 2004;42(2):90-93
OBJECTIVETo study the effect of macrophage inflammatory protein-1alpha(MIP-1alpha) and its mRNA on airway inflammation of mouse with induced asthma.
METHODSSeventy male BALB/C mice were randomly divided into the control group and asthma group (including 7 subgroups, 10 mice each). The control group included group A(24) (the lavaging subgroup was sacrificed 24 h after the last challenge) and group A(0) (the non-lavaging subgroup was sacrificed from 18 h to 24 h after the last challenge); asthma group included group B(3) (the lavaging subgroup was sacrificed 3 h after the last challenge), group B(8) (the lavaging subgroup was sacrificed 8 h after the last challenge), group B(24) (the lavaging subgroup was sacrificed 24 h after the last challenge), group B(36) (the lavaging subgroup was sacrificed 36 h after the last challenge) and group B(0) (the non-lavaging subgroup was sacrificed from 18 h to 24 h after the last challenge). In the experiment, the mice model of asthma was established by the ovalbumin (OVA) challenge methods. Eosinophils (EOS) numbers and differentiated cell numbers in bronchoalveolar lavage fluid (BALF) were counted; the concentrations of MIP-1alpha in serum and BALF were measured by sandwich enzyme-linked immunosorbent assay (sandwich ELISA); the protein expressions of MIP-1alpha were detected by immunohistochemical techniques; the mRNA expressions of MIP-1alpha were determined by in situ hybridization technique.
RESULTS(1) The concentrations of MIP-1alpha in BALF and serum of group B(3) [(30.2 +/- 4.2) pg/ml, (30.8 +/- 4.6) pg/ml], group B(8) [(35.3 +/- 4.9) pg/ml, (34.9 +/- 5.1) pg/ml], group B(24) [(42.9 +/- 5.8) pg/ml, (41.7 +/- 6.3) pg/ml] and group B(36) [(37.8 +/- 4.7) pg/ml, (35.7 +/- 4.9) pg/ml] were significantly higher than those of group A(24) [(20.9 +/- 3.8) pg/ml, (22.4 +/- 4.3) pg/ml] (P < 0.01); the concentrations of MIP-1alpha in BALF and serum went up at 3 h, reached peak at 24 h, and had descended at 36 h. (2) Immunohistochemistry showed that the protein expressions of MIP-1alpha around the bronchus of group B(0) [(26.4 +/- 6.2)%] were significantly elevated as compared to those of group A(0) [(10.3 +/- 2.5)%] (P < 0.01), the epithelial cell was the chief expression cell. (3) In situ hybridization showed that the mRNA expressions of MIP-1alpha around the bronchus of group B(0) [(23.9 +/- 4.2)%] were significantly increased when compared to those of group A(0) [(8.7 +/- 1.8)%] (P < 0.01), the epithelial cell was the chief expression cell. (4) There was a significant correlation between the concentrations of MIP-1alpha and the numbers of EOS in BALF and between the concentrations of MIP-1alpha and the percentage of EOS numbers in the total cell numbers (EOS%) in BALF.
CONCLUSIONSMIP-1alpha protein and MIP-1alpha mRNA were found strongly expressed in mouse asthma model, the epithelial cell was the chief expression cell; the kinetic characteristic of MIP-1alpha showed that its level increased at 3 h, reached peak at 24 h and declined at 36 h; MIP-1alpha and EOS gathering had a significant correlation.
Animals ; Asthma ; blood ; genetics ; Bronchoalveolar Lavage Fluid ; chemistry ; Chemokine CCL3 ; Chemokine CCL4 ; Disease Models, Animal ; Enzyme-Linked Immunosorbent Assay ; In Situ Hybridization ; Macrophage Inflammatory Proteins ; blood ; genetics ; Male ; Mice ; Mice, Inbred BALB C ; RNA, Messenger ; genetics ; metabolism
4.Effect of xiaoai jiedu recipe on gene expression profiles in H22 tumor-bearing mice.
Chinese Journal of Integrated Traditional and Western Medicine 2013;33(9):1232-1235
OBJECTIVETo explore the mechanism of Xiaoai Jiedu Recipe (XJR) for fighting against tumors by detecting tumor gene expression profiles of H22 tumor-bearing mice.
METHODSH22 tumor-bearing mice were randomly divided into the normal control group, the low dose XJR group, the medium dose XJR group, the high dose XJR group, and the Cisplatin group. The differentially expressed genes of tumor tissues in H22 tumor-bearing mice were detected by using gene chip technique. The antitumor mechanism of XJR associated signaling pathways and gene expressions were found out by pathway analysis. The chemokine signaling pathways were analyzed.
RESULTSXJP could significantly affect multiple signaling pathways associated with tumor growth, apoptosis, and immunity. XJP also could decrease expressions of CCL3 and CXCL2 in the chemokine signaling pathway.
CONCLUSIONXJP could inhibit the growth and invasion of tumor cells possibly by affecting expressions of some genes in the chemokine signaling pathway.
Animals ; Cell Line, Tumor ; Chemokine CCL3 ; metabolism ; Chemokine CXCL2 ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; Gene Expression Profiling ; Liver Neoplasms, Experimental ; genetics ; metabolism ; Mice ; Mice, Inbred ICR ; Signal Transduction ; drug effects
5.Expression of macrophage inflammatory protein 1 alpha in the endothelial cells exposed to diamide.
Limin YANG ; Xuewei ZHU ; Xia ZHAO ; Zhongduan DENG
Journal of Huazhong University of Science and Technology (Medical Sciences) 2003;23(3):219-233
In order to study whether the endothelial cells (ECs) with lipid peroxidation induced by diamide can express and secrete macrophage inflammatory protein 1 alpha (MIP-1 alpha), the expression of MIP-1 alpha protein in the cells was detected by cell enzyme-linked immunosorbent assay (ELISA) and that of MIP-1 alpha mRNA was determined by cell in situ hybridization and nuclease S1 protection assay after the ECs were exposed to different concentrations of diamide for 4 h. The chemotactic activity of MIP-1 alpha was tested by micropore filter method using modified Boyden chambers. Cell ELISA showed that the expression of MIP-1 alpha protein in endothelial cells exposed to 1 mumol/L, 5 mumol/L and 10 mumol/L diamide was 1.9-fold, 2.3-fold and 1.7-fold respectively as much as that in the control cells, which was statistically significant by analysis of variance. In situ hybridization revealed that the mRNA expression of ECs treated with 1 mumol/L, 5 mumol/L and 10 mumol/L diamide was 1.3-fold, 3.0-fold and 1.7-fold as much as that in the control group, which had statistical significance (F = 188.93, P < 0.01). The mRNA expression in 5 mumol/L dimide treated ECs, measured by nuclease S1 protection assay, was 3.4-fold as much as that in the control group (t = 8.70, P < 0.05). Chemotactic response(99.50 +/- 4.31 microns) to the culture medium conditioned by 5 mumol/L diamide treated ECs, which was stronger than that(66.47 +/- 3.25 microns) conditioned by the ECs (F = 404.31, P < 0.05), was significantly decreased (F = 192.25, P < 0.05) after adding MIP-1 alpha antibody. It suggests that diamide, a lipid peroxidation inducer, could stimulate ECs to produce high level of MIP-1 alpha, and might play an important role in atherogenesis by promoting the migration of peripheral blood monocytes into arterial intima.
Cells, Cultured
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Chemokine CCL3
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Chemokine CCL4
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Chemotaxis, Leukocyte
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physiology
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Diamide
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pharmacology
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Endothelium, Vascular
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cytology
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metabolism
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Humans
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Lipid Peroxidation
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Macrophage Inflammatory Proteins
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biosynthesis
;
genetics
;
RNA, Messenger
;
biosynthesis
;
genetics
;
Sulfhydryl Reagents
;
pharmacology
;
Umbilical Veins
;
cytology
6.Lipopolysaccharide induces expression of macrophage inflammatory protein-1alpha in human umbilical vein endothelial cells.
Zhong-duan DENG ; Zhi-ling QU ; Li-min YANG
Chinese Journal of Pathology 2003;32(5):449-452
OBJECTIVETo understand whether endotoxin lipopolysaccharide (LPS) is able to induce the expression of macrophage inflammatory protein-1alpha (MIP-1alpha) mRNA and protein in human umbilical vein endothelial cells (HUVECs).
METHODSThe expression of MIP-1alpha mRNA was determined by dot blotting analysis and by in situ hybridization using a digoxigenin-labeled MIP-1alpha cDNA probe after exposure of the cultured HUVECs to LPS at different concentrations. The expression of MIP-1alpha mRNA was determined by RT-PCR as well. In addition, the expression of MIP-1alpha protein was tested by cell enzyme-linked immunosorbent assay (ELISA) using a goat anti-human monoclonal MIP-1alpha antibody.
RESULTSDot blotting showed that the absorbance values of the dots on the nitrocellulose membrane were 1.490 and 3.310 when exposed to LPS at the concentrations of 1 micro g/ml and 10 micro g/ml which were 1.97- and 4.38-fold over that of the control group (0.775), respectively. In situ hybridization revealed that exposure to LPS at a concentration of 1 micro g/ml led to a significant increase in the MIP-1alpha mRNA expression in HUVECs as compared to the control group (F = 142.83, P < 0.01), whereas the MIP-1alpha mRNA in HUVECs was somewhat decreased when exposed to LPS at a concentration of 10 micro g/ml. RT-PCR revealed that the expression of MIP-1alpha mRNA in HUVECs were 1.65-, 2.86- and 1.26-fold over that of the control group when exposed to LPS at the concentrations of 1 micro g/ml, 5 micro g/ml and 10 micro g/ml respectively. Cell ELISA showed that after exposure of the HUVECs to LPS at the concentrations mentioned above, the expression of MIP-1alpha protein was strongly increased, especially in the 5 micro g/ml LPS group. Analysis of variance showed that there was a significant difference between groups (F = 15.36, P < 0.05).
CONCLUSIONSLPS may induce a high level of MIP-1alpha mRNA and protein expression in HUVECs, and it might, hereby, play an important role in the recruitment of the monocytes/macrophages into the arterial intima.
Cells, Cultured ; Chemokine CCL3 ; Chemokine CCL4 ; Endothelial Cells ; drug effects ; metabolism ; Enzyme-Linked Immunosorbent Assay ; Gene Expression Regulation ; drug effects ; Humans ; In Situ Hybridization ; Lipopolysaccharides ; toxicity ; Macrophage Inflammatory Proteins ; analysis ; genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Umbilical Veins ; drug effects
7.Gene Expression Profiles in Genetically Different Mice Infected with Toxoplasma gondii: ALDH1A2, BEX2, EGR2, CCL3 and PLAU.
Hassan Ahmed Hassan Ahmed ISMAIL ; Juan Hua QUAN ; Zhou WEI ; In Wook CHOI ; Guang Ho CHA ; Dae Whan SHIN ; Young Ha LEE ; Chang June SONG
The Korean Journal of Parasitology 2012;50(1):7-13
Toxoplasma gondii can modulate host cell gene expression; however, determining gene expression levels in intermediate hosts after T. gondii infection is not known much. We selected 5 genes (ALDH1A2, BEX2, CCL3, EGR2 and PLAU) and compared the mRNA expression levels in the spleen, liver, lung and small intestine of genetically different mice infected with T. gondii. ALDH1A2 mRNA expressions of both mouse strains were markedly increased at day 1-4 postinfection (PI) and then decreased, and its expressions in the spleen and lung were significantly higher in C57BL/6 mice than those of BALB/c mice. BEX2 and CCR3 mRNA expressions of both mouse strains were significantly increased from day 7 PI and peaked at day 15-30 PI (P<0.05), especially high in the spleen liver or small intestine of C57BL/6 mice. EGR2 and PLAU mRNA expressions of both mouse strains were significantly increased after infection, especially high in the spleen and liver. However, their expression patterns were varied depending on the tissue and mouse strain. Taken together, T. gondii-susceptible C57BL/6 mice expressed higher levels of these 5 genes than did T. gondii-resistant BALB/c mice, particularly in the spleen and liver. And ALDH1A2 and PLAU expressions were increased acutely, whereas BEX2, CCL3 and EGR2 expressions were increased lately. Thus, these demonstrate that host genetic factors exert a strong impact on the expression of these 5 genes and their expression patterns were varied depending on the gene or tissue.
Aldehyde Dehydrogenase/*genetics/metabolism
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Animals
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Brain/metabolism/parasitology
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Chemokine CCL3/*genetics/metabolism
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Early Growth Response Protein 2/*genetics/metabolism
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Gene Expression Profiling
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Humans
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Lung/metabolism/parasitology
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Mice
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Mice, Inbred BALB C
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Mice, Inbred C57BL
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Mice, Inbred Strains
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Nerve Tissue Proteins/*genetics/metabolism
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Organ Specificity
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Spleen/metabolism/virology
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Toxoplasma/*physiology
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Toxoplasmosis/*genetics/metabolism/parasitology
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Urokinase-Type Plasminogen Activator/*genetics/metabolism
8.Homocysteine induces macrophage inflammatory protein-1alpha expression by activating NF-kappaB in THP-1 monocytes.
Wei XING ; Zhong-Duan DENG ; Zhi-Ling QU ; Juan NI
Chinese Journal of Pathology 2005;34(2):101-104
OBJECTIVETo investigate the effect of homocysteine (HCY) on activation of nuclear factor (NF-kappaB) and inhibitory factor IkappaB-alpha in human monocyte cell line THP-1, as well as its association with macrophage inflammatory protein (MIP-1alpha) upregulation.
METHODSTHP-1 monocytes were incubated with HCY, with and without NF-kappaB inhibitor pyrolidine dithiocarbamate (PDTC) pretreatment. Northern blot analysis and flow cytometry were used to detect MIP-1alpha mRNA and protein respectively. The nuclear protein NF-kappaB P65 subunit and the inhibitory protein IkappaB-alpha were analyzed by Western blotting.
RESULTSCompared with controls, HCY, at a concentration of 0.1 mmol/L, was able to enhance the expression of MIP-1alpha mRNA (up to 3.69-fold) and protein (1.16-fold) in THP-1 monocytes, as well as enhance NF-kappaB P65 transcription to nuclear proteins. These actions were significantly suppressed after pretreatment with 100 micromol/L PDTC for 30 minutes before HCY incubation; whereas incubation of THP-1 monocytes with PDTC only had no effect on both the expression of MIP-1alpha and nuclear transcription of NF-kappaB P65. Moreover, the level of IkappaB-alpha protein in THP-1 monocytes decreased after a 30-minute incubation with HCY, which gradually increased after 120 minutes.
CONCLUSIONSHomocysteine at a pathologic concentration stimulates MIP-1alpha expression in THP-1 monocytes, probably via NF-kappaB activation. Such activation may be caused by enhanced phosphorylation and degradation of the inhibitor protein IkappaB-alpha.
Cell Line, Tumor ; Chemokine CCL3 ; Chemokine CCL4 ; Homocysteine ; pharmacology ; Humans ; I-kappa B Proteins ; metabolism ; Leukemia, Monocytic, Acute ; metabolism ; pathology ; Macrophage Inflammatory Proteins ; biosynthesis ; genetics ; Monocytes ; metabolism ; NF-KappaB Inhibitor alpha ; NF-kappa B ; antagonists & inhibitors ; Phosphorylation ; Proline ; analogs & derivatives ; pharmacology ; RNA, Messenger ; biosynthesis ; genetics ; Thiocarbamates ; pharmacology ; Transcription Factor RelA ; biosynthesis ; genetics ; Transcription, Genetic
9.Immune response of melanoma antigen gene-3 modified dendritic cell vaccines in gastric carcinoma.
Song-bing HE ; Liang WANG ; Yan-yun ZHANG
Chinese Journal of Oncology 2009;31(5):330-334
OBJECTIVETo investigate the anti-gastric carcinoma immunological efficacy of dendritic cells (DC) precursors, that were mobilized into the peripheral blood by injection of macrophage inflammation protein-1 alpha (MIP-1 alpha), and induced by DC vaccine expressing melanoma antigen gene-3 (MAGE-3) ex vivo and in vivo.
METHODS615 mice were injected with MIP-1 alpha via the tail vein. Freshly isolated B220(-) CD11c+ cells were cultured with cytokines and assayed by phenotype analysis and mixed lymphocyte reaction (MLR). For adenoviral (Ad)-mediated gene transduction, cultured B220(-) CD11c+ cells were incubated with Ad-melanoma antigen gene-3. MIP-1 alpha-mobilized B220(-) CD11c+ cells pulsed MFC cells tumor lysate were used as positive control. The stimulated DC vaccination-induced T lymphocytes, and the killing effect of the T cells on gastric carcinoma cells were assayed by MTT. INF-gamma production was determined with the INF-gamma ELISA kit. To establish the solid tumor model, groups of 615 mice were injected with MFC cells subcutaneously into the abdominal wall. MIP-1 alpha-mobilized DC vaccines expressing MAGE-3 gene were used to immunize the mice after the challenge of MFC cells, then the tumor size and the survival of mice were examined to detect the therapeutic effect of DC vaccines.
RESULTSB220(-) CD11c+ cells increased obviously after MIP-1 alpha injection, and freshly isolated B220(-) CD11c+ cells cultured with mGM-CSF, IL-4, and mTNF-alpha were phenotypically identical to typical DC, gained the capacity to stimulate allogeneic T cells. These MIP-1 alpha-mobilized DCs were transduced with Ad-MAGE-3, which were prepared for DC vaccines expressing tumor antigen. T lymphocytes stimulated with DC-transduced with Ad-MAGE-3 showed specific killing effect on gastric carcinoma cells and produced high levels of INF-gamma [(1460.00 +/- 16.82) pg/ml]. Five days after the MFC cells challenge, the mice were subsequently injected with DC vaccines. The tumor size of the experimental group was significantly smaller than that in the positive control group and the negative control groups (P<0.01). Kaplan-Meier survival curves showed the survival of the experimental group mice was significantly longer than that of the control groups (P<0.01).
CONCLUSIONB220(-) CD11c+ DC precursors are rapidly accumulated in the peripheral blood after injection of MIP-1 alpha into mice, which can further differentiate into mature DCs. These MIP-1 alpha-mobilized DCs, when transduced with MAGE-3 gene, can induce specific CTL to gastric carcinoma cells ex vivo, and can generate anti-tumor therapeutic effects on MFC cells loading mice in vivo. The efficiency of anti-tumor therapeutic immunity induced by MIP-1 alpha-mobilized DCs expressing tumor antigen are much more potent than MIP-1 alpha mobilized DCs pulsed MFC cells tumor lysate.
Adenoviridae ; genetics ; Animals ; Antigens, Neoplasm ; genetics ; metabolism ; Cancer Vaccines ; therapeutic use ; Cell Line, Tumor ; Cell Proliferation ; Chemokine CCL3 ; metabolism ; pharmacology ; Dendritic Cells ; metabolism ; Female ; Interferon-gamma ; metabolism ; Mice ; Mice, Inbred BALB C ; Neoplasm Proteins ; genetics ; metabolism ; Stomach Neoplasms ; metabolism ; pathology ; therapy ; T-Lymphocytes ; cytology ; metabolism ; T-Lymphocytes, Cytotoxic ; cytology ; metabolism ; Transduction, Genetic
10.Protective effect of 4,4'-diaminodiphenylsulfone against paraquat-induced mouse lung injury.
Sung Chun CHO ; Ji Heon RHIM ; Hae Ri CHOI ; Young Hoon SON ; Seok Jin LEE ; Kye Yong SONG ; Sang Chul PARK
Experimental & Molecular Medicine 2011;43(9):525-537
Although 4,4'-diaminodiphenylsulfone (DDS, dapsone) has been used to treat several dermatologic conditions, including Hansen disease, for the past several decades, its mode of action has remained a topic of debate. We recently reported that DDS treatment significantly extends the lifespan of the nematode C. elegans by decreasing the generation of reactive oxygen species. Additionally, in in vitro experiments using non-phagocytic human fibroblasts, we found that DDS effectively counteracted the toxicity of paraquat (PQ). In the present study, we extended our work to test the protective effect of DDS against PQ in vivo using a mouse lung injury model. Oral administration of DDS to mice significantly attenuated the lung tissue damage caused by subsequent administration of PQ. Moreover, DDS reduced the local expression of mRNA transcripts encoding inflammation-related molecules, including endothelin-1 (ET-1), macrophage inflammatory protein-1alpha (MIP-1alpha), and transforming growth factor-beta (TGF-beta). In addition, DDS decreased the PQ-induced expression of NADPH oxidase mRNA and activation of protein kinase Cmicro (PKCmicro). DDS treatment also decreased the PQ-induced generation of superoxide anions in mouse lung fibroblasts. Taken together, these data suggest the novel efficacy of DDS as an effective protective agent against oxidative stress-induced tissue damages.
Animals
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Cells, Cultured
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Chemokine CCL3/drug effects/metabolism
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Dapsone/*administration & dosage
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Endothelin-1/drug effects/metabolism
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Fibroblasts/drug effects
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Herbicides/*antagonists & inhibitors/toxicity
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Lung Injury/chemically induced/*prevention & control
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Male
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Mice
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Mice, Inbred BALB C
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Oxidative Stress
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Paraquat/*antagonists & inhibitors/toxicity
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Protective Agents/*administration & dosage
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Protein Kinase C/genetics/metabolism
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Superoxides/analysis
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Transforming Growth Factor beta/drug effects/metabolism