Molecular interactions that enable movement of the Lyme disease agent from the tick gut into the hemolymph
Borrelia burgdorferi, the causative agent of Lyme disease, is transmitted to humans by bite of Ixodes scapularis ticks. The mechanisms by which the bacterium is transmitted from vector to host are poorly understood. In this study, we show that the F(ab)(2) fragments of BBE31, a B.burgdorferi outer-s...
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| creator | Zhang, Lili Zhang, Yue Adusumilli, Sarojini Liu, Lei Narasimhan, Sukanya Dai, Jianfeng Zhao, Yang O Fikrig, Erol |
| description | Borrelia burgdorferi, the causative agent of Lyme disease, is transmitted to humans by bite of Ixodes scapularis ticks. The mechanisms by which the bacterium is transmitted from vector to host are poorly understood. In this study, we show that the F(ab)(2) fragments of BBE31, a B.burgdorferi outer-surface lipoprotein, interfere with the migration of the spirochete from tick gut into the hemolymph during tick feeding. The decreased hemolymph infection results in lower salivary glands infection, and consequently attenuates mouse infection by tick-transmitted B. burgdorferi. Using a yeast surface display approach, a tick gut protein named TRE31 was identified to interact with BBE31. Silencing tre31 also decreased the B. burgdorferi burden in the tick hemolymph. Delineating the specific spirochete and arthropod ligands required for B. burgdorferi movement in the tick may lead to new strategies to interrupt the life cycle of the Lyme disease agent. |
| doi_str_mv | 10.1371/journal.ppat.1002079 |
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The mechanisms by which the bacterium is transmitted from vector to host are poorly understood. In this study, we show that the F(ab)(2) fragments of BBE31, a B.burgdorferi outer-surface lipoprotein, interfere with the migration of the spirochete from tick gut into the hemolymph during tick feeding. The decreased hemolymph infection results in lower salivary glands infection, and consequently attenuates mouse infection by tick-transmitted B. burgdorferi. Using a yeast surface display approach, a tick gut protein named TRE31 was identified to interact with BBE31. Silencing tre31 also decreased the B. burgdorferi burden in the tick hemolymph. Delineating the specific spirochete and arthropod ligands required for B. burgdorferi movement in the tick may lead to new strategies to interrupt the life cycle of the Lyme disease agent.</description><identifier>ISSN: 1553-7374</identifier><identifier>ISSN: 1553-7366</identifier><identifier>EISSN: 1553-7374</identifier><identifier>DOI: 10.1371/journal.ppat.1002079</identifier><identifier>PMID: 21695244</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Bacterial Outer Membrane Proteins ; Borrelia burgdorferi - pathogenicity ; Care and treatment ; Diagnosis ; Gastrointestinal Tract - microbiology ; Gene expression ; Genes ; Hemolymph - microbiology ; Lipoproteins ; Lyme disease ; Lyme Disease - microbiology ; Medicine ; Microbiota (Symbiotic organisms) ; Molecular Sequence Data ; Movement ; Parasites ; Physiological aspects ; Plasmids ; Polymerase chain reaction ; Proteins ; Ticks - microbiology</subject><ispartof>PLoS pathogens, 2011-06, Vol.7 (6), p.e1002079-e1002079</ispartof><rights>COPYRIGHT 2011 Public Library of Science</rights><rights>2011 Zhang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Zhang L, Zhang Y, Adusumilli S, Liu L, Narasimhan S, et al. (2011) Molecular Interactions that Enable Movement of the Lyme Disease Agent from the Tick Gut into the Hemolymph. 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The mechanisms by which the bacterium is transmitted from vector to host are poorly understood. In this study, we show that the F(ab)(2) fragments of BBE31, a B.burgdorferi outer-surface lipoprotein, interfere with the migration of the spirochete from tick gut into the hemolymph during tick feeding. The decreased hemolymph infection results in lower salivary glands infection, and consequently attenuates mouse infection by tick-transmitted B. burgdorferi. Using a yeast surface display approach, a tick gut protein named TRE31 was identified to interact with BBE31. Silencing tre31 also decreased the B. burgdorferi burden in the tick hemolymph. Delineating the specific spirochete and arthropod ligands required for B. burgdorferi movement in the tick may lead to new strategies to interrupt the life cycle of the Lyme disease agent.</description><subject>Animals</subject><subject>Bacterial Outer Membrane Proteins</subject><subject>Borrelia burgdorferi - pathogenicity</subject><subject>Care and treatment</subject><subject>Diagnosis</subject><subject>Gastrointestinal Tract - microbiology</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Hemolymph - microbiology</subject><subject>Lipoproteins</subject><subject>Lyme disease</subject><subject>Lyme Disease - microbiology</subject><subject>Medicine</subject><subject>Microbiota (Symbiotic organisms)</subject><subject>Molecular Sequence Data</subject><subject>Movement</subject><subject>Parasites</subject><subject>Physiological aspects</subject><subject>Plasmids</subject><subject>Polymerase chain reaction</subject><subject>Proteins</subject><subject>Ticks - microbiology</subject><issn>1553-7374</issn><issn>1553-7366</issn><issn>1553-7374</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqVkk2P0zAQhiMEYpeFf4AgEgfEocVfiZ0L0mrFR6UCEh9ny3HGaYoTF9tZ0X-P02ZXW7QX5IOtmWdez7yaLHuO0RJTjt9u3egHZZe7nYpLjBBBvHqQneOioAtOOXt4532WPQlhixDDFJePszOCy6ogjJ1n28_Ogh6t8nk3RPBKx84NIY8bFXMYVG0h79019DDE3JkUh3y97yFvugAqQK7aKWO86w-52OlfeTvGSc0dIhvond33u83T7JFRNsCz-b7Ifn54_-Pq02L99ePq6nK90GWJ4gIAowYZbWpBVcENKxmreaWLmjKutRACI-AGC8a5QKpCNaEFAV5xnaZTiF5kL4-6O-uCnG0KEhNRJZvKkiZidSQap7Zy57te-b10qpOHgPOtVD5NYkHWhBAoC1YYkdowuG4QJjUjHAvKRWWS1rv5t7HuodHJDa_siehpZug2snXXkmKMCzY183oW8O73CCHKvgsarFUDuDFIwSmrCoZYIl_9Q94_3Ey1KvXfDcalb_WkKS9JiZKcqCat5T1UOg30nXYDmC7FTwrenBQkJsKf2KoxBLn6_u0_2C-nLDuy2rsQPJhb6zCS06LfDCmnRZfzoqeyF3dtvy262Wz6F-OZ-H8</recordid><startdate>20110601</startdate><enddate>20110601</enddate><creator>Zhang, Lili</creator><creator>Zhang, Yue</creator><creator>Adusumilli, Sarojini</creator><creator>Liu, Lei</creator><creator>Narasimhan, Sukanya</creator><creator>Dai, Jianfeng</creator><creator>Zhao, Yang O</creator><creator>Fikrig, Erol</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>ISN</scope><scope>ISR</scope><scope>3V.</scope><scope>7QL</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</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>C1K</scope><scope>CCPQU</scope><scope>DWQXO</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>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20110601</creationdate><title>Molecular interactions that enable movement of the Lyme disease agent from the tick gut into the hemolymph</title><author>Zhang, Lili ; Zhang, Yue ; Adusumilli, Sarojini ; Liu, Lei ; Narasimhan, Sukanya ; Dai, Jianfeng ; Zhao, Yang O ; Fikrig, Erol</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c660t-ee10d0fcfb83a57f4644b79c5b347cc88810e7f1847780a90b2352e797c131a03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Bacterial Outer Membrane Proteins</topic><topic>Borrelia burgdorferi - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PLoS pathogens</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Lili</au><au>Zhang, Yue</au><au>Adusumilli, Sarojini</au><au>Liu, Lei</au><au>Narasimhan, Sukanya</au><au>Dai, Jianfeng</au><au>Zhao, Yang O</au><au>Fikrig, Erol</au><au>Sacks, David L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Molecular interactions that enable movement of the Lyme disease agent from the tick gut into the hemolymph</atitle><jtitle>PLoS pathogens</jtitle><addtitle>PLoS Pathog</addtitle><date>2011-06-01</date><risdate>2011</risdate><volume>7</volume><issue>6</issue><spage>e1002079</spage><epage>e1002079</epage><pages>e1002079-e1002079</pages><issn>1553-7374</issn><issn>1553-7366</issn><eissn>1553-7374</eissn><abstract>Borrelia burgdorferi, the causative agent of Lyme disease, is transmitted to humans by bite of Ixodes scapularis ticks. The mechanisms by which the bacterium is transmitted from vector to host are poorly understood. In this study, we show that the F(ab)(2) fragments of BBE31, a B.burgdorferi outer-surface lipoprotein, interfere with the migration of the spirochete from tick gut into the hemolymph during tick feeding. The decreased hemolymph infection results in lower salivary glands infection, and consequently attenuates mouse infection by tick-transmitted B. burgdorferi. Using a yeast surface display approach, a tick gut protein named TRE31 was identified to interact with BBE31. Silencing tre31 also decreased the B. burgdorferi burden in the tick hemolymph. Delineating the specific spirochete and arthropod ligands required for B. burgdorferi movement in the tick may lead to new strategies to interrupt the life cycle of the Lyme disease agent.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>21695244</pmid><doi>10.1371/journal.ppat.1002079</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Bacterial Outer Membrane Proteins Borrelia burgdorferi - pathogenicity Care and treatment Diagnosis Gastrointestinal Tract - microbiology Gene expression Genes Hemolymph - microbiology Lipoproteins Lyme disease Lyme Disease - microbiology Medicine Microbiota (Symbiotic organisms) Molecular Sequence Data Movement Parasites Physiological aspects Plasmids Polymerase chain reaction Proteins Ticks - microbiology |
| title | Molecular interactions that enable movement of the Lyme disease agent from the tick gut into the hemolymph |
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