Human C-C chemokine receptor 3 monoclonal antibody inhibits pulmonary inflammation in allergic mice
Aim： To evaluate the effect of C-C chemokine receptor 3 （CCR3） blockade on pulmonary inflammation and mucus production in allergic mice. Methods： We used the synthetic peptide of the CCR3 NH2-terminal as the immunizing antigen and generated murine monoclonal antibody against the human CCR3. In addit...
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| Veröffentlicht in: | Acta pharmacologica Sinica 2007-11, Vol.28 (11), p.1791-1796 |
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| creator | Wang, Kai Shen, Hua-hao Li, Wen Huang, Hua-qiong |
| description | Aim： To evaluate the effect of C-C chemokine receptor 3 （CCR3） blockade on pulmonary inflammation and mucus production in allergic mice. Methods： We used the synthetic peptide of the CCR3 NH2-terminal as the immunizing antigen and generated murine monoclonal antibody against the human CCR3. In addition, the generated antibody was administered to mice sensitized and challenged with ovalbumin. The inflammatory cells in bronchoalveolar lavage, cytokine levels, pulmonary histopathology, and mucus secretion were examined. Results： The Western blotting analysis indicated that the generated antibody bound to CCR3 specifically. The allergic mice treated with the antihuman CCR3 antibody exhibited a significant reduction of pulmonary inflammation accompanied with the alteration of cytokine. Conclusion： The antibody we generated was specific to CCR3. The inhibition of airway inflammation and mucus overproduction by the antibody suggested that the blockade of CCR3 is an appealing therapeutical target for asthma. The present research may provide an experimental basis for the further study of this agent. |
| doi_str_mv | 10.1111/j.1745-7254.2007.00635.x |
| format | Article |
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Methods： We used the synthetic peptide of the CCR3 NH2-terminal as the immunizing antigen and generated murine monoclonal antibody against the human CCR3. In addition, the generated antibody was administered to mice sensitized and challenged with ovalbumin. The inflammatory cells in bronchoalveolar lavage, cytokine levels, pulmonary histopathology, and mucus secretion were examined. Results： The Western blotting analysis indicated that the generated antibody bound to CCR3 specifically. The allergic mice treated with the antihuman CCR3 antibody exhibited a significant reduction of pulmonary inflammation accompanied with the alteration of cytokine. Conclusion： The antibody we generated was specific to CCR3. The inhibition of airway inflammation and mucus overproduction by the antibody suggested that the blockade of CCR3 is an appealing therapeutical target for asthma. The present research may provide an experimental basis for the further study of this agent.</description><identifier>ISSN: 1671-4083</identifier><identifier>EISSN: 1745-7254</identifier><identifier>DOI: 10.1111/j.1745-7254.2007.00635.x</identifier><identifier>PMID: 17959030</identifier><language>eng</language><publisher>United States: Nature Publishing Group</publisher><subject>Animals ; Antibodies, Monoclonal - biosynthesis ; Antibodies, Monoclonal - pharmacology ; Bronchoalveolar Lavage Fluid - chemistry ; Bronchoalveolar Lavage Fluid - cytology ; Bronchoalveolar Lavage Fluid - immunology ; Cytokines - analysis ; Male ; Mice ; Mice, Inbred BALB C ; Mucus - secretion ; Ovalbumin ; Pneumonia - chemically induced ; Pneumonia - metabolism ; Receptors, CCR3 - immunology ; Respiratory Hypersensitivity - chemically induced ; Respiratory Hypersensitivity - immunology ; 白细胞介素</subject><ispartof>Acta pharmacologica Sinica, 2007-11, Vol.28 (11), p.1791-1796</ispartof><rights>Copyright Nature Publishing Group Nov 2007</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/95561A/95561A.jpg</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17959030$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Kai</creatorcontrib><creatorcontrib>Shen, Hua-hao</creatorcontrib><creatorcontrib>Li, Wen</creatorcontrib><creatorcontrib>Huang, Hua-qiong</creatorcontrib><title>Human C-C chemokine receptor 3 monoclonal antibody inhibits pulmonary inflammation in allergic mice</title><title>Acta pharmacologica Sinica</title><addtitle>Acta Pharmacologica Sinica</addtitle><description>Aim： To evaluate the effect of C-C chemokine receptor 3 （CCR3） blockade on pulmonary inflammation and mucus production in allergic mice. Methods： We used the synthetic peptide of the CCR3 NH2-terminal as the immunizing antigen and generated murine monoclonal antibody against the human CCR3. In addition, the generated antibody was administered to mice sensitized and challenged with ovalbumin. The inflammatory cells in bronchoalveolar lavage, cytokine levels, pulmonary histopathology, and mucus secretion were examined. Results： The Western blotting analysis indicated that the generated antibody bound to CCR3 specifically. The allergic mice treated with the antihuman CCR3 antibody exhibited a significant reduction of pulmonary inflammation accompanied with the alteration of cytokine. Conclusion： The antibody we generated was specific to CCR3. The inhibition of airway inflammation and mucus overproduction by the antibody suggested that the blockade of CCR3 is an appealing therapeutical target for asthma. The present research may provide an experimental basis for the further study of this agent.</description><subject>Animals</subject><subject>Antibodies, Monoclonal - biosynthesis</subject><subject>Antibodies, Monoclonal - pharmacology</subject><subject>Bronchoalveolar Lavage Fluid - chemistry</subject><subject>Bronchoalveolar Lavage Fluid - cytology</subject><subject>Bronchoalveolar Lavage Fluid - immunology</subject><subject>Cytokines - analysis</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mucus - secretion</subject><subject>Ovalbumin</subject><subject>Pneumonia - chemically induced</subject><subject>Pneumonia - metabolism</subject><subject>Receptors, CCR3 - immunology</subject><subject>Respiratory Hypersensitivity - chemically induced</subject><subject>Respiratory Hypersensitivity - immunology</subject><subject>白细胞介素</subject><issn>1671-4083</issn><issn>1745-7254</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kMlKxEAQhhtR3F9BGg96Sqzek6MMbiB40XPodDozPfYyZgF9e1vcwIN1qPXjh_oRwgRKkuNiXRLFRaGo4CUFUCWAZKJ83UL7P4ft3EtFCg4V20MH47gGYJSRehftEVWLGhjsI3M7Bx3xolhgs7IhPbto8WCN3UxpwAyHFJPxKWqPdZxcm7o37OLKtW4a8Wb2-a6Hj1XvdQh6cinmAWvv7bB0Bgdn7BHa6bUf7fFXPURP11ePi9vi_uHmbnF5XxhG5VRYzm3PjRKcVpIAWKBWA_SU1pTJnLu6pcJ0pCVCyb7uWwmVMZWo8l8dk-wQnX_qbob0MttxaoIbjfVeR5vmsVFZREFFVCbP_iUpCEFrQTN4-gdcp3nIbmSGMCCcyCpDJ1_Q3AbbNZvBhWxK8-3yr4pZpbh8cXHZtNo8987bhgrFVUWBvQOdYop7</recordid><startdate>20071101</startdate><enddate>20071101</enddate><creator>Wang, Kai</creator><creator>Shen, Hua-hao</creator><creator>Li, Wen</creator><creator>Huang, Hua-qiong</creator><general>Nature Publishing Group</general><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>W91</scope><scope>~WA</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7QO</scope></search><sort><creationdate>20071101</creationdate><title>Human C-C chemokine receptor 3 monoclonal antibody inhibits pulmonary inflammation in allergic mice</title><author>Wang, Kai ; Shen, Hua-hao ; Li, Wen ; Huang, Hua-qiong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c326t-e44ef4c754286100e02ea00f229236229d9b25cd1b1576f9fb608cc858032d363</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Antibodies, Monoclonal - biosynthesis</topic><topic>Antibodies, Monoclonal - pharmacology</topic><topic>Bronchoalveolar Lavage Fluid - chemistry</topic><topic>Bronchoalveolar Lavage Fluid - cytology</topic><topic>Bronchoalveolar Lavage Fluid - immunology</topic><topic>Cytokines - analysis</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mucus - secretion</topic><topic>Ovalbumin</topic><topic>Pneumonia - chemically induced</topic><topic>Pneumonia - metabolism</topic><topic>Receptors, CCR3 - immunology</topic><topic>Respiratory Hypersensitivity - chemically induced</topic><topic>Respiratory Hypersensitivity - immunology</topic><topic>白细胞介素</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Kai</creatorcontrib><creatorcontrib>Shen, Hua-hao</creatorcontrib><creatorcontrib>Li, Wen</creatorcontrib><creatorcontrib>Huang, Hua-qiong</creatorcontrib><collection>中文科技期刊数据库</collection><collection>中文科技期刊数据库-CALIS站点</collection><collection>中文科技期刊数据库-7.0平台</collection><collection>中文科技期刊数据库-医药卫生</collection><collection>中文科技期刊数据库- 镜像站点</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Biotechnology Research Abstracts</collection><jtitle>Acta pharmacologica Sinica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Kai</au><au>Shen, Hua-hao</au><au>Li, Wen</au><au>Huang, Hua-qiong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Human C-C chemokine receptor 3 monoclonal antibody inhibits pulmonary inflammation in allergic mice</atitle><jtitle>Acta pharmacologica Sinica</jtitle><addtitle>Acta Pharmacologica Sinica</addtitle><date>2007-11-01</date><risdate>2007</risdate><volume>28</volume><issue>11</issue><spage>1791</spage><epage>1796</epage><pages>1791-1796</pages><issn>1671-4083</issn><eissn>1745-7254</eissn><abstract>Aim： To evaluate the effect of C-C chemokine receptor 3 （CCR3） blockade on pulmonary inflammation and mucus production in allergic mice. Methods： We used the synthetic peptide of the CCR3 NH2-terminal as the immunizing antigen and generated murine monoclonal antibody against the human CCR3. In addition, the generated antibody was administered to mice sensitized and challenged with ovalbumin. The inflammatory cells in bronchoalveolar lavage, cytokine levels, pulmonary histopathology, and mucus secretion were examined. Results： The Western blotting analysis indicated that the generated antibody bound to CCR3 specifically. The allergic mice treated with the antihuman CCR3 antibody exhibited a significant reduction of pulmonary inflammation accompanied with the alteration of cytokine. Conclusion： The antibody we generated was specific to CCR3. The inhibition of airway inflammation and mucus overproduction by the antibody suggested that the blockade of CCR3 is an appealing therapeutical target for asthma. 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| subjects | Animals Antibodies, Monoclonal - biosynthesis Antibodies, Monoclonal - pharmacology Bronchoalveolar Lavage Fluid - chemistry Bronchoalveolar Lavage Fluid - cytology Bronchoalveolar Lavage Fluid - immunology Cytokines - analysis Male Mice Mice, Inbred BALB C Mucus - secretion Ovalbumin Pneumonia - chemically induced Pneumonia - metabolism Receptors, CCR3 - immunology Respiratory Hypersensitivity - chemically induced Respiratory Hypersensitivity - immunology 白细胞介素 |
| title | Human C-C chemokine receptor 3 monoclonal antibody inhibits pulmonary inflammation in allergic mice |
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