Plasminogen-Activating Protease Specifically Controls the Development of Primary Pneumonic Plague
Primary pneumonic plague is transmitted easily, progresses rapidly, and causes high mortality, but the mechanisms by which Yersinia pestis overwhelms the lungs are largely unknown. We show that the plasminogen activator Pla is essential for Y. pestis to cause primary pneumonic plague but is less imp...
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| Veröffentlicht in: | Science (American Association for the Advancement of Science) 2007-01, Vol.315 (5811), p.509-513 |
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| creator | Lathem, Wyndham W Price, Paul A Miller, Virginia L Goldman, William E |
| description | Primary pneumonic plague is transmitted easily, progresses rapidly, and causes high mortality, but the mechanisms by which Yersinia pestis overwhelms the lungs are largely unknown. We show that the plasminogen activator Pla is essential for Y. pestis to cause primary pneumonic plague but is less important for dissemination during pneumonic plague than during bubonic plague. Experiments manipulating its temporal expression showed that Pla allows Y. pestis to replicate rapidly in the airways, causing a lethal fulminant pneumonia; if unexpressed, inflammation is aborted, and lung repair is activated. Inhibition of Pla expression prolonged the survival of animals with the disease, offering a therapeutic option to extend the period during which antibiotics are effective. |
| doi_str_mv | 10.1126/science.1137195 |
| format | Article |
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We show that the plasminogen activator Pla is essential for Y. pestis to cause primary pneumonic plague but is less important for dissemination during pneumonic plague than during bubonic plague. Experiments manipulating its temporal expression showed that Pla allows Y. pestis to replicate rapidly in the airways, causing a lethal fulminant pneumonia; if unexpressed, inflammation is aborted, and lung repair is activated. Inhibition of Pla expression prolonged the survival of animals with the disease, offering a therapeutic option to extend the period during which antibiotics are effective.</description><identifier>ISSN: 0036-8075</identifier><identifier>EISSN: 1095-9203</identifier><identifier>DOI: 10.1126/science.1137195</identifier><identifier>PMID: 17255510</identifier><identifier>CODEN: SCIEAS</identifier><language>eng</language><publisher>Washington, DC: American Association for the Advancement of Science</publisher><subject>Animals ; Bacteria ; Bacterial diseases ; Bacteriology ; Biological and medical sciences ; Cell Proliferation ; Colony Count, Microbial ; Cytokines ; Cytokines - genetics ; Cytokines - metabolism ; Female ; Fibrinogen - metabolism ; Fundamental and applied biological sciences. 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We show that the plasminogen activator Pla is essential for Y. pestis to cause primary pneumonic plague but is less important for dissemination during pneumonic plague than during bubonic plague. Experiments manipulating its temporal expression showed that Pla allows Y. pestis to replicate rapidly in the airways, causing a lethal fulminant pneumonia; if unexpressed, inflammation is aborted, and lung repair is activated. Inhibition of Pla expression prolonged the survival of animals with the disease, offering a therapeutic option to extend the period during which antibiotics are effective.</description><subject>Animals</subject><subject>Bacteria</subject><subject>Bacterial diseases</subject><subject>Bacteriology</subject><subject>Biological and medical sciences</subject><subject>Cell Proliferation</subject><subject>Colony Count, Microbial</subject><subject>Cytokines</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Female</subject><subject>Fibrinogen - metabolism</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>Gene Expression Regulation, Bacterial</subject><subject>Human bacterial diseases</subject><subject>Infections</subject><subject>Infectious diseases</subject><subject>Inflammation</subject><subject>Inhibitor drugs</subject><subject>Lung - immunology</subject><subject>Lung - microbiology</subject><subject>Lung - pathology</subject><subject>Lung diseases</subject><subject>Lungs</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Microbiology</subject><subject>Mutation</subject><subject>Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains</subject><subject>Pathogens</subject><subject>Pharmacology</subject><subject>Plague</subject><subject>Plague - immunology</subject><subject>Plague - microbiology</subject><subject>Plague - pathology</subject><subject>Plasminogen - metabolism</subject><subject>Plasminogen Activators - genetics</subject><subject>Plasminogen Activators - metabolism</subject><subject>Pneumonia, Bacterial - immunology</subject><subject>Pneumonia, Bacterial - microbiology</subject><subject>Pneumonia, Bacterial - pathology</subject><subject>Pneumonic plague</subject><subject>Proteases</subject><subject>Spleen</subject><subject>Spleen - microbiology</subject><subject>Tetracyclines - pharmacology</subject><subject>Tropical bacterial diseases</subject><subject>Virulence</subject><subject>Virulence Factors - genetics</subject><subject>Virulence Factors - metabolism</subject><subject>Yersinia pestis</subject><subject>Yersinia pestis - enzymology</subject><subject>Yersinia pestis - genetics</subject><subject>Yersinia pestis - growth & development</subject><subject>Yersinia pestis - pathogenicity</subject><issn>0036-8075</issn><issn>1095-9203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFksFrFDEUxoModq2ePamDUG9jX5LJTHIsq1Wh4ELrOWSzL2uWmWRNZgr9780ygwUvPSXh_d7H994XQt5S-Ewpay-z9RgslgfvqBLPyIqCErViwJ-TFQBvawmdOCOvcj4AlJriL8kZ7ZgQgsKKmE1v8uBD3GOor-zo783ow77apDiiyVjdHtF6563p-4dqHcOYYp-r8TdWX_Ae-3gcMIxVdKXDDyY9VJuA0xCDt1WR3k_4mrxwps_4ZjnPyd3117v19_rm57cf66ub2jYKxnoL1jSNZU7QrpWtANUwwxw40SjLectgh13DTbFteHHPtw7Lxe0kE9I0_Jx8mmWPKf6ZMI968Nli35uAccq6lapRjMKTIG-pYEw9rVj2zaDtTuDH_8BDnFIow2pGedk4l6pAlzNkU8w5odPHeWGagj5lqZcs9ZJl6Xi_yE7bAXeP_BJeAS4WwOSSj0smWJ8fOSlAtMAL927mDnmM6V-dle8hJT9Z-zDXnYna7FPR-HXLgHKArqG8SPwFYIC6Tg</recordid><startdate>20070126</startdate><enddate>20070126</enddate><creator>Lathem, Wyndham W</creator><creator>Price, Paul A</creator><creator>Miller, Virginia L</creator><creator>Goldman, William E</creator><general>American Association for the Advancement of Science</general><general>The American Association for the Advancement of Science</general><scope>FBQ</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>7QF</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QQ</scope><scope>7QR</scope><scope>7SC</scope><scope>7SE</scope><scope>7SN</scope><scope>7SP</scope><scope>7SR</scope><scope>7SS</scope><scope>7T7</scope><scope>7TA</scope><scope>7TB</scope><scope>7TK</scope><scope>7TM</scope><scope>7U5</scope><scope>7U9</scope><scope>8BQ</scope><scope>8FD</scope><scope>C1K</scope><scope>F28</scope><scope>FR3</scope><scope>H8D</scope><scope>H8G</scope><scope>H94</scope><scope>JG9</scope><scope>JQ2</scope><scope>K9.</scope><scope>KR7</scope><scope>L7M</scope><scope>L~C</scope><scope>L~D</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7T5</scope><scope>7X8</scope></search><sort><creationdate>20070126</creationdate><title>Plasminogen-Activating Protease Specifically Controls the Development of Primary Pneumonic Plague</title><author>Lathem, Wyndham W ; Price, Paul A ; Miller, Virginia L ; Goldman, William E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c490t-b0ca44c2f51768650942a2f0f549c33620de743a551a32553bfea32fd8258a43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Bacteria</topic><topic>Bacterial diseases</topic><topic>Bacteriology</topic><topic>Biological and medical sciences</topic><topic>Cell Proliferation</topic><topic>Colony Count, Microbial</topic><topic>Cytokines</topic><topic>Cytokines - genetics</topic><topic>Cytokines - metabolism</topic><topic>Female</topic><topic>Fibrinogen - metabolism</topic><topic>Fundamental and applied biological sciences. 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Academic</collection><jtitle>Science (American Association for the Advancement of Science)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lathem, Wyndham W</au><au>Price, Paul A</au><au>Miller, Virginia L</au><au>Goldman, William E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Plasminogen-Activating Protease Specifically Controls the Development of Primary Pneumonic Plague</atitle><jtitle>Science (American Association for the Advancement of Science)</jtitle><addtitle>Science</addtitle><date>2007-01-26</date><risdate>2007</risdate><volume>315</volume><issue>5811</issue><spage>509</spage><epage>513</epage><pages>509-513</pages><issn>0036-8075</issn><eissn>1095-9203</eissn><coden>SCIEAS</coden><abstract>Primary pneumonic plague is transmitted easily, progresses rapidly, and causes high mortality, but the mechanisms by which Yersinia pestis overwhelms the lungs are largely unknown. We show that the plasminogen activator Pla is essential for Y. pestis to cause primary pneumonic plague but is less important for dissemination during pneumonic plague than during bubonic plague. Experiments manipulating its temporal expression showed that Pla allows Y. pestis to replicate rapidly in the airways, causing a lethal fulminant pneumonia; if unexpressed, inflammation is aborted, and lung repair is activated. Inhibition of Pla expression prolonged the survival of animals with the disease, offering a therapeutic option to extend the period during which antibiotics are effective.</abstract><cop>Washington, DC</cop><pub>American Association for the Advancement of Science</pub><pmid>17255510</pmid><doi>10.1126/science.1137195</doi><tpages>5</tpages></addata></record> |
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| subjects | Animals Bacteria Bacterial diseases Bacteriology Biological and medical sciences Cell Proliferation Colony Count, Microbial Cytokines Cytokines - genetics Cytokines - metabolism Female Fibrinogen - metabolism Fundamental and applied biological sciences. Psychology Gene expression Gene Expression Regulation Gene Expression Regulation, Bacterial Human bacterial diseases Infections Infectious diseases Inflammation Inhibitor drugs Lung - immunology Lung - microbiology Lung - pathology Lung diseases Lungs Medical sciences Mice Mice, Inbred C57BL Microbiology Mutation Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains Pathogens Pharmacology Plague Plague - immunology Plague - microbiology Plague - pathology Plasminogen - metabolism Plasminogen Activators - genetics Plasminogen Activators - metabolism Pneumonia, Bacterial - immunology Pneumonia, Bacterial - microbiology Pneumonia, Bacterial - pathology Pneumonic plague Proteases Spleen Spleen - microbiology Tetracyclines - pharmacology Tropical bacterial diseases Virulence Virulence Factors - genetics Virulence Factors - metabolism Yersinia pestis Yersinia pestis - enzymology Yersinia pestis - genetics Yersinia pestis - growth & development Yersinia pestis - pathogenicity |
| title | Plasminogen-Activating Protease Specifically Controls the Development of Primary Pneumonic Plague |
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