Expression of Chemokines and Induction of Rapid Cell Death in Human Blood Neutrophils by Mycobacterium tuberculosis
To elucidate the role of neutrophils in the early inflammatory response to mycobacterial infection, expression of chemokines interleukin (IL)-8 and macrophage inflammatory protein-1α (MIP-1α) was examined in human blood neutrophils in response to the lipopolysaccharide (LPS) of Escherichia coli, whi...
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| Veröffentlicht in: | The Journal of infectious diseases 1998-07, Vol.178 (1), p.127-137 |
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| creator | Kasahara, Keita Sato, Ikuyo Ogura, Keiichi Takeuchi, Hiroko Kobayashi, Kazuo Adachi, Mitsuru |
| description | To elucidate the role of neutrophils in the early inflammatory response to mycobacterial infection, expression of chemokines interleukin (IL)-8 and macrophage inflammatory protein-1α (MIP-1α) was examined in human blood neutrophils in response to the lipopolysaccharide (LPS) of Escherichia coli, which induces acute inflammation, or to Mycobacterium tuberculosis or purified protein derivative (PPD), which induce chronic mycobacterial inflammation. Neutrophils stimulated with LPS, M. tuberculosis, or PPD expressed both IL-8 and MIP-1α. Expression of IL-8 and MIP-1α was lower after stimulation with M. tuberculosis or PPD than after stimulation with LPS, but the kinetics of expression did not differ significantly. In contrast, both M. tuberculosis and PPD with tumor necrosis factor-α induced neutrophils to undergo rapid cell death, which might remove neutrophils and activate macrophages at sites of mycobacterial inflammation. The findings suggest that neutrophils play important roles in the host defense against mycobacterial infection. |
| doi_str_mv | 10.1086/515585 |
| format | Article |
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Neutrophils stimulated with LPS, M. tuberculosis, or PPD expressed both IL-8 and MIP-1α. Expression of IL-8 and MIP-1α was lower after stimulation with M. tuberculosis or PPD than after stimulation with LPS, but the kinetics of expression did not differ significantly. In contrast, both M. tuberculosis and PPD with tumor necrosis factor-α induced neutrophils to undergo rapid cell death, which might remove neutrophils and activate macrophages at sites of mycobacterial inflammation. The findings suggest that neutrophils play important roles in the host defense against mycobacterial infection.</description><identifier>ISSN: 0022-1899</identifier><identifier>EISSN: 1537-6613</identifier><identifier>DOI: 10.1086/515585</identifier><identifier>PMID: 9652432</identifier><identifier>CODEN: JIDIAQ</identifier><language>eng</language><publisher>Chicago, IL: The University of Chicago Press</publisher><subject>Analysis of the immune response. 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Neutrophils stimulated with LPS, M. tuberculosis, or PPD expressed both IL-8 and MIP-1α. Expression of IL-8 and MIP-1α was lower after stimulation with M. tuberculosis or PPD than after stimulation with LPS, but the kinetics of expression did not differ significantly. In contrast, both M. tuberculosis and PPD with tumor necrosis factor-α induced neutrophils to undergo rapid cell death, which might remove neutrophils and activate macrophages at sites of mycobacterial inflammation. The findings suggest that neutrophils play important roles in the host defense against mycobacterial infection.</description><subject>Analysis of the immune response. Humoral and cellular immunity</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Cell death</subject><subject>Cell Survival</subject><subject>Cells, Cultured</subject><subject>Chemokine CCL3</subject><subject>Chemokine CCL4</subject><subject>Chemokines</subject><subject>Cytokines</subject><subject>Dose-Response Relationship, Drug</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>Humans</subject><subject>Immunobiology</subject><subject>Immunoenzyme Techniques</subject><subject>Inflammation</subject><subject>Interleukin-1 - pharmacology</subject><subject>Interleukin-8 - biosynthesis</subject><subject>Interleukin-8 - genetics</subject><subject>Lipopolysaccharides - immunology</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Lymphokines, interleukins ( function, expression)</subject><subject>Macrophage Inflammatory Proteins - biosynthesis</subject><subject>Macrophage Inflammatory Proteins - genetics</subject><subject>Macrophages</subject><subject>Major Articles</subject><subject>Messenger RNA</subject><subject>Mycobacterium tuberculosis</subject><subject>Mycobacterium tuberculosis - immunology</subject><subject>Neutrophils</subject><subject>Neutrophils - cytology</subject><subject>Neutrophils - immunology</subject><subject>Regulatory factors and their cellular receptors</subject><subject>RNA, Messenger</subject><subject>Time Factors</subject><subject>Tuberculin</subject><subject>Tuberculin - immunology</subject><subject>Tuberculin - pharmacology</subject><subject>Tuberculosis</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><issn>0022-1899</issn><issn>1537-6613</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkV1rFDEUhoModa36D4Qg4t1oPiaTyaXdtm5Lq_gFpTchyZxhs52ZrMkEuv--U3ZYxRuvDuF5eDknL0KvKflASV19FFSIWjxBCyq4LKqK8qdoQQhjBa2Veo5epLQhhJS8kkfoSFWClZwtUDq730ZIyYcBhxYv19CHOz9AwmZo8MXQZDfO7LvZ-gYvoevwKZhxjf2AV7k3Az7pQmjwF8hjDNu17xK2O3y9c8EaN0L0ucdjthBd7kLy6SV61pouwat5HqNf52c_l6vi6uvni-Wnq8KVgo8FGCUbsLJWvKqFhRZIqaB14KC0pbTMypJSBZyK0klXW2lbIw1xzfQGLvkxer_P3cbwO0Made-Tm_Y3A4SctFSqnn7k_yKtREW4ehTf_iNuQo7DdIRmjCtaUs7_pLkYUorQ6m30vYk7TYl-7Ervu5rEN3Natj00B20uZ-LvZm6SM10bzeB8OmiMCyrZXzGbNIZ4wJzQaR9WTbzYc59GuD9wE-90JbkUenVzq69_fLs8vbnl-pI_AAiqtDo</recordid><startdate>19980701</startdate><enddate>19980701</enddate><creator>Kasahara, Keita</creator><creator>Sato, Ikuyo</creator><creator>Ogura, Keiichi</creator><creator>Takeuchi, Hiroko</creator><creator>Kobayashi, Kazuo</creator><creator>Adachi, Mitsuru</creator><general>The University of Chicago Press</general><general>University of Chicago Press</general><general>Oxford University Press</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7QL</scope><scope>C1K</scope><scope>7X8</scope></search><sort><creationdate>19980701</creationdate><title>Expression of Chemokines and Induction of Rapid Cell Death in Human Blood Neutrophils by Mycobacterium tuberculosis</title><author>Kasahara, Keita ; Sato, Ikuyo ; Ogura, Keiichi ; Takeuchi, Hiroko ; Kobayashi, Kazuo ; Adachi, Mitsuru</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c453t-ea97deb7893685befe049efcece4b47b2b74119e3154c7c8b7bfa7a0cd54ce373</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Analysis of the immune response. Humoral and cellular immunity</topic><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>Cell death</topic><topic>Cell Survival</topic><topic>Cells, Cultured</topic><topic>Chemokine CCL3</topic><topic>Chemokine CCL4</topic><topic>Chemokines</topic><topic>Cytokines</topic><topic>Dose-Response Relationship, Drug</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fundamental immunology</topic><topic>Humans</topic><topic>Immunobiology</topic><topic>Immunoenzyme Techniques</topic><topic>Inflammation</topic><topic>Interleukin-1 - pharmacology</topic><topic>Interleukin-8 - biosynthesis</topic><topic>Interleukin-8 - genetics</topic><topic>Lipopolysaccharides - immunology</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Lymphokines, interleukins ( function, expression)</topic><topic>Macrophage Inflammatory Proteins - biosynthesis</topic><topic>Macrophage Inflammatory Proteins - genetics</topic><topic>Macrophages</topic><topic>Major Articles</topic><topic>Messenger RNA</topic><topic>Mycobacterium tuberculosis</topic><topic>Mycobacterium tuberculosis - immunology</topic><topic>Neutrophils</topic><topic>Neutrophils - cytology</topic><topic>Neutrophils - immunology</topic><topic>Regulatory factors and their cellular receptors</topic><topic>RNA, Messenger</topic><topic>Time Factors</topic><topic>Tuberculin</topic><topic>Tuberculin - immunology</topic><topic>Tuberculin - pharmacology</topic><topic>Tuberculosis</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kasahara, Keita</creatorcontrib><creatorcontrib>Sato, Ikuyo</creatorcontrib><creatorcontrib>Ogura, Keiichi</creatorcontrib><creatorcontrib>Takeuchi, Hiroko</creatorcontrib><creatorcontrib>Kobayashi, Kazuo</creatorcontrib><creatorcontrib>Adachi, Mitsuru</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of infectious diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kasahara, Keita</au><au>Sato, Ikuyo</au><au>Ogura, Keiichi</au><au>Takeuchi, Hiroko</au><au>Kobayashi, Kazuo</au><au>Adachi, Mitsuru</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression of Chemokines and Induction of Rapid Cell Death in Human Blood Neutrophils by Mycobacterium tuberculosis</atitle><jtitle>The Journal of infectious diseases</jtitle><addtitle>J Infect Dis</addtitle><date>1998-07-01</date><risdate>1998</risdate><volume>178</volume><issue>1</issue><spage>127</spage><epage>137</epage><pages>127-137</pages><issn>0022-1899</issn><eissn>1537-6613</eissn><coden>JIDIAQ</coden><abstract>To elucidate the role of neutrophils in the early inflammatory response to mycobacterial infection, expression of chemokines interleukin (IL)-8 and macrophage inflammatory protein-1α (MIP-1α) was examined in human blood neutrophils in response to the lipopolysaccharide (LPS) of Escherichia coli, which induces acute inflammation, or to Mycobacterium tuberculosis or purified protein derivative (PPD), which induce chronic mycobacterial inflammation. Neutrophils stimulated with LPS, M. tuberculosis, or PPD expressed both IL-8 and MIP-1α. Expression of IL-8 and MIP-1α was lower after stimulation with M. tuberculosis or PPD than after stimulation with LPS, but the kinetics of expression did not differ significantly. In contrast, both M. tuberculosis and PPD with tumor necrosis factor-α induced neutrophils to undergo rapid cell death, which might remove neutrophils and activate macrophages at sites of mycobacterial inflammation. The findings suggest that neutrophils play important roles in the host defense against mycobacterial infection.</abstract><cop>Chicago, IL</cop><pub>The University of Chicago Press</pub><pmid>9652432</pmid><doi>10.1086/515585</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Analysis of the immune response. Humoral and cellular immunity Apoptosis Biological and medical sciences Cell death Cell Survival Cells, Cultured Chemokine CCL3 Chemokine CCL4 Chemokines Cytokines Dose-Response Relationship, Drug Fundamental and applied biological sciences. Psychology Fundamental immunology Humans Immunobiology Immunoenzyme Techniques Inflammation Interleukin-1 - pharmacology Interleukin-8 - biosynthesis Interleukin-8 - genetics Lipopolysaccharides - immunology Lipopolysaccharides - pharmacology Lymphokines, interleukins ( function, expression) Macrophage Inflammatory Proteins - biosynthesis Macrophage Inflammatory Proteins - genetics Macrophages Major Articles Messenger RNA Mycobacterium tuberculosis Mycobacterium tuberculosis - immunology Neutrophils Neutrophils - cytology Neutrophils - immunology Regulatory factors and their cellular receptors RNA, Messenger Time Factors Tuberculin Tuberculin - immunology Tuberculin - pharmacology Tuberculosis Tumor Necrosis Factor-alpha - pharmacology |
| title | Expression of Chemokines and Induction of Rapid Cell Death in Human Blood Neutrophils by Mycobacterium tuberculosis |
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