Loading…
Resistance to Lyme disease in decorin-deficient mice
Microbial adhesion to the host tissue represents an early, critical step in the pathogenesis of most infectious diseases. BORRELIA: burgdorferi, the causative agent of Lyme disease (LD), expresses two surface-exposed decorin-binding adhesins, DbpA and DbpB. A decorin-deficient (Dcn(-/-)) mouse was r...
Saved in:
Published in: | The Journal of clinical investigation 2001-04, Vol.107 (7), p.845-852 |
---|---|
Main Authors: | , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
cited_by | cdi_FETCH-LOGICAL-c437t-1ce192c084996aa6dfc360f5d53ab6be4b7f3b6b5b70d130200df01a2d1f9c963 |
---|---|
cites | cdi_FETCH-LOGICAL-c437t-1ce192c084996aa6dfc360f5d53ab6be4b7f3b6b5b70d130200df01a2d1f9c963 |
container_end_page | 852 |
container_issue | 7 |
container_start_page | 845 |
container_title | The Journal of clinical investigation |
container_volume | 107 |
creator | Brown, E L Wooten, R M Johnson, B J Iozzo, R V Smith, A Dolan, M C Guo, B P Weis, J J Höök, M |
description | Microbial adhesion to the host tissue represents an early, critical step in the pathogenesis of most infectious diseases. BORRELIA: burgdorferi, the causative agent of Lyme disease (LD), expresses two surface-exposed decorin-binding adhesins, DbpA and DbpB. A decorin-deficient (Dcn(-/-)) mouse was recently developed and found to have a relatively mild phenotype. We have now examined the process of experimental LD in Dcn(-/-) mice using both needle inoculation and tick transmission of spirochetes. When exposed to low doses of the infective agent, Dcn(-/-) mice had fewer Borrelia-positive cultures from most tissues analyzed than did Dcn(+/+) or Dcn(+/-) mice. When the infection dose was increased, similar differences were not observed in most tissues but were seen in bacterial colonization of joints and the extent of Borreila-induced arthritis. Quantitative PCR demonstrated that joints harvested from Dcn(-/-) mice had diminished Borrelia numbers compared with issues harvested from Dcn(+/+) controls. Histological examination also revealed a low incidence and severity of arthritis in Dcn(-/-) mice. Conversely, no differences in the numbers of Borreila-positive skin cultures were observed among the different genotypes regardless of the infection dose. These differences, which were observed regardless of genetic background of the mice (BALB/c or C3H/HeN) or method of infection, demonstrate the importance of decorin in the pathogenesis of LD. |
doi_str_mv | 10.1172/JCI11692 |
format | article |
fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_199574</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>18253312</sourcerecordid><originalsourceid>FETCH-LOGICAL-c437t-1ce192c084996aa6dfc360f5d53ab6be4b7f3b6b5b70d130200df01a2d1f9c963</originalsourceid><addsrcrecordid>eNqFkM1LAzEQxXNQbK2Cf4HsSbysZpLsZnPwIKVqpSCInkM2mWhkP-pmK_S_d0vr18nTPJjfm3k8Qk6AXgBIdnk_nQPkiu2RMaUMUiV5MSKHMb5RCkJk4oCMAFiRccrHRDxiDLE3jcWkb5PFusbEhYgmYhKaxKFtu9CkDn2wAZs-qYPFI7LvTRXxeDcn5Plm9jS9SxcPt_Pp9SK1gss-BYugmKWFUCo3Jnfe8pz6zGXclHmJopSeDyIrJXXAKaPUeQqGOfDKqpxPyNX27nJV1ujs8L8zlV52oTbdWrcm6L-bJrzql_ZDg1KZFIP_bOfv2vcVxl7XIVqsKtNgu4paSsq4EOxfEAqWcQ4b8HwL2q6NsUP_HQao3tSvv-of0NPf4X_AXff8EzKrgbE</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>18253312</pqid></control><display><type>article</type><title>Resistance to Lyme disease in decorin-deficient mice</title><source>PubMed Central Free</source><source>EZB-FREE-00999 freely available EZB journals</source><creator>Brown, E L ; Wooten, R M ; Johnson, B J ; Iozzo, R V ; Smith, A ; Dolan, M C ; Guo, B P ; Weis, J J ; Höök, M</creator><creatorcontrib>Brown, E L ; Wooten, R M ; Johnson, B J ; Iozzo, R V ; Smith, A ; Dolan, M C ; Guo, B P ; Weis, J J ; Höök, M</creatorcontrib><description>Microbial adhesion to the host tissue represents an early, critical step in the pathogenesis of most infectious diseases. BORRELIA: burgdorferi, the causative agent of Lyme disease (LD), expresses two surface-exposed decorin-binding adhesins, DbpA and DbpB. A decorin-deficient (Dcn(-/-)) mouse was recently developed and found to have a relatively mild phenotype. We have now examined the process of experimental LD in Dcn(-/-) mice using both needle inoculation and tick transmission of spirochetes. When exposed to low doses of the infective agent, Dcn(-/-) mice had fewer Borrelia-positive cultures from most tissues analyzed than did Dcn(+/+) or Dcn(+/-) mice. When the infection dose was increased, similar differences were not observed in most tissues but were seen in bacterial colonization of joints and the extent of Borreila-induced arthritis. Quantitative PCR demonstrated that joints harvested from Dcn(-/-) mice had diminished Borrelia numbers compared with issues harvested from Dcn(+/+) controls. Histological examination also revealed a low incidence and severity of arthritis in Dcn(-/-) mice. Conversely, no differences in the numbers of Borreila-positive skin cultures were observed among the different genotypes regardless of the infection dose. These differences, which were observed regardless of genetic background of the mice (BALB/c or C3H/HeN) or method of infection, demonstrate the importance of decorin in the pathogenesis of LD.</description><identifier>ISSN: 0021-9738</identifier><identifier>DOI: 10.1172/JCI11692</identifier><identifier>PMID: 11285303</identifier><language>eng</language><publisher>United States: American Society for Clinical Investigation</publisher><subject>adhesins ; Animals ; Borrelia burgdorferi ; Borrelia burgdorferi Group - immunology ; Borrelia burgdorferi Group - pathogenicity ; DbpA protein ; DbpB protein ; Decorin ; Disease Models, Animal ; Extracellular Matrix Proteins ; Female ; Immunity, Innate ; Ixodes ; Lyme Disease - immunology ; Lyme Disease - microbiology ; Lyme Disease - pathology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Knockout ; Proteoglycans - genetics ; Proteoglycans - immunology ; Proteoglycans - physiology</subject><ispartof>The Journal of clinical investigation, 2001-04, Vol.107 (7), p.845-852</ispartof><rights>Copyright © 2001, American Society for Clinical Investigation 2001</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c437t-1ce192c084996aa6dfc360f5d53ab6be4b7f3b6b5b70d130200df01a2d1f9c963</citedby><cites>FETCH-LOGICAL-c437t-1ce192c084996aa6dfc360f5d53ab6be4b7f3b6b5b70d130200df01a2d1f9c963</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC199574/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC199574/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11285303$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Brown, E L</creatorcontrib><creatorcontrib>Wooten, R M</creatorcontrib><creatorcontrib>Johnson, B J</creatorcontrib><creatorcontrib>Iozzo, R V</creatorcontrib><creatorcontrib>Smith, A</creatorcontrib><creatorcontrib>Dolan, M C</creatorcontrib><creatorcontrib>Guo, B P</creatorcontrib><creatorcontrib>Weis, J J</creatorcontrib><creatorcontrib>Höök, M</creatorcontrib><title>Resistance to Lyme disease in decorin-deficient mice</title><title>The Journal of clinical investigation</title><addtitle>J Clin Invest</addtitle><description>Microbial adhesion to the host tissue represents an early, critical step in the pathogenesis of most infectious diseases. BORRELIA: burgdorferi, the causative agent of Lyme disease (LD), expresses two surface-exposed decorin-binding adhesins, DbpA and DbpB. A decorin-deficient (Dcn(-/-)) mouse was recently developed and found to have a relatively mild phenotype. We have now examined the process of experimental LD in Dcn(-/-) mice using both needle inoculation and tick transmission of spirochetes. When exposed to low doses of the infective agent, Dcn(-/-) mice had fewer Borrelia-positive cultures from most tissues analyzed than did Dcn(+/+) or Dcn(+/-) mice. When the infection dose was increased, similar differences were not observed in most tissues but were seen in bacterial colonization of joints and the extent of Borreila-induced arthritis. Quantitative PCR demonstrated that joints harvested from Dcn(-/-) mice had diminished Borrelia numbers compared with issues harvested from Dcn(+/+) controls. Histological examination also revealed a low incidence and severity of arthritis in Dcn(-/-) mice. Conversely, no differences in the numbers of Borreila-positive skin cultures were observed among the different genotypes regardless of the infection dose. These differences, which were observed regardless of genetic background of the mice (BALB/c or C3H/HeN) or method of infection, demonstrate the importance of decorin in the pathogenesis of LD.</description><subject>adhesins</subject><subject>Animals</subject><subject>Borrelia burgdorferi</subject><subject>Borrelia burgdorferi Group - immunology</subject><subject>Borrelia burgdorferi Group - pathogenicity</subject><subject>DbpA protein</subject><subject>DbpB protein</subject><subject>Decorin</subject><subject>Disease Models, Animal</subject><subject>Extracellular Matrix Proteins</subject><subject>Female</subject><subject>Immunity, Innate</subject><subject>Ixodes</subject><subject>Lyme Disease - immunology</subject><subject>Lyme Disease - microbiology</subject><subject>Lyme Disease - pathology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Inbred C3H</subject><subject>Mice, Knockout</subject><subject>Proteoglycans - genetics</subject><subject>Proteoglycans - immunology</subject><subject>Proteoglycans - physiology</subject><issn>0021-9738</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><recordid>eNqFkM1LAzEQxXNQbK2Cf4HsSbysZpLsZnPwIKVqpSCInkM2mWhkP-pmK_S_d0vr18nTPJjfm3k8Qk6AXgBIdnk_nQPkiu2RMaUMUiV5MSKHMb5RCkJk4oCMAFiRccrHRDxiDLE3jcWkb5PFusbEhYgmYhKaxKFtu9CkDn2wAZs-qYPFI7LvTRXxeDcn5Plm9jS9SxcPt_Pp9SK1gss-BYugmKWFUCo3Jnfe8pz6zGXclHmJopSeDyIrJXXAKaPUeQqGOfDKqpxPyNX27nJV1ujs8L8zlV52oTbdWrcm6L-bJrzql_ZDg1KZFIP_bOfv2vcVxl7XIVqsKtNgu4paSsq4EOxfEAqWcQ4b8HwL2q6NsUP_HQao3tSvv-of0NPf4X_AXff8EzKrgbE</recordid><startdate>20010401</startdate><enddate>20010401</enddate><creator>Brown, E L</creator><creator>Wooten, R M</creator><creator>Johnson, B J</creator><creator>Iozzo, R V</creator><creator>Smith, A</creator><creator>Dolan, M C</creator><creator>Guo, B P</creator><creator>Weis, J J</creator><creator>Höök, M</creator><general>American Society for Clinical Investigation</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>7QL</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20010401</creationdate><title>Resistance to Lyme disease in decorin-deficient mice</title><author>Brown, E L ; Wooten, R M ; Johnson, B J ; Iozzo, R V ; Smith, A ; Dolan, M C ; Guo, B P ; Weis, J J ; Höök, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c437t-1ce192c084996aa6dfc360f5d53ab6be4b7f3b6b5b70d130200df01a2d1f9c963</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>adhesins</topic><topic>Animals</topic><topic>Borrelia burgdorferi</topic><topic>Borrelia burgdorferi Group - immunology</topic><topic>Borrelia burgdorferi Group - pathogenicity</topic><topic>DbpA protein</topic><topic>DbpB protein</topic><topic>Decorin</topic><topic>Disease Models, Animal</topic><topic>Extracellular Matrix Proteins</topic><topic>Female</topic><topic>Immunity, Innate</topic><topic>Ixodes</topic><topic>Lyme Disease - immunology</topic><topic>Lyme Disease - microbiology</topic><topic>Lyme Disease - pathology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Inbred C3H</topic><topic>Mice, Knockout</topic><topic>Proteoglycans - genetics</topic><topic>Proteoglycans - immunology</topic><topic>Proteoglycans - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Brown, E L</creatorcontrib><creatorcontrib>Wooten, R M</creatorcontrib><creatorcontrib>Johnson, B J</creatorcontrib><creatorcontrib>Iozzo, R V</creatorcontrib><creatorcontrib>Smith, A</creatorcontrib><creatorcontrib>Dolan, M C</creatorcontrib><creatorcontrib>Guo, B P</creatorcontrib><creatorcontrib>Weis, J J</creatorcontrib><creatorcontrib>Höök, M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of clinical investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Brown, E L</au><au>Wooten, R M</au><au>Johnson, B J</au><au>Iozzo, R V</au><au>Smith, A</au><au>Dolan, M C</au><au>Guo, B P</au><au>Weis, J J</au><au>Höök, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Resistance to Lyme disease in decorin-deficient mice</atitle><jtitle>The Journal of clinical investigation</jtitle><addtitle>J Clin Invest</addtitle><date>2001-04-01</date><risdate>2001</risdate><volume>107</volume><issue>7</issue><spage>845</spage><epage>852</epage><pages>845-852</pages><issn>0021-9738</issn><abstract>Microbial adhesion to the host tissue represents an early, critical step in the pathogenesis of most infectious diseases. BORRELIA: burgdorferi, the causative agent of Lyme disease (LD), expresses two surface-exposed decorin-binding adhesins, DbpA and DbpB. A decorin-deficient (Dcn(-/-)) mouse was recently developed and found to have a relatively mild phenotype. We have now examined the process of experimental LD in Dcn(-/-) mice using both needle inoculation and tick transmission of spirochetes. When exposed to low doses of the infective agent, Dcn(-/-) mice had fewer Borrelia-positive cultures from most tissues analyzed than did Dcn(+/+) or Dcn(+/-) mice. When the infection dose was increased, similar differences were not observed in most tissues but were seen in bacterial colonization of joints and the extent of Borreila-induced arthritis. Quantitative PCR demonstrated that joints harvested from Dcn(-/-) mice had diminished Borrelia numbers compared with issues harvested from Dcn(+/+) controls. Histological examination also revealed a low incidence and severity of arthritis in Dcn(-/-) mice. Conversely, no differences in the numbers of Borreila-positive skin cultures were observed among the different genotypes regardless of the infection dose. These differences, which were observed regardless of genetic background of the mice (BALB/c or C3H/HeN) or method of infection, demonstrate the importance of decorin in the pathogenesis of LD.</abstract><cop>United States</cop><pub>American Society for Clinical Investigation</pub><pmid>11285303</pmid><doi>10.1172/JCI11692</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0021-9738 |
ispartof | The Journal of clinical investigation, 2001-04, Vol.107 (7), p.845-852 |
issn | 0021-9738 |
language | eng |
recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_199574 |
source | PubMed Central Free; EZB-FREE-00999 freely available EZB journals |
subjects | adhesins Animals Borrelia burgdorferi Borrelia burgdorferi Group - immunology Borrelia burgdorferi Group - pathogenicity DbpA protein DbpB protein Decorin Disease Models, Animal Extracellular Matrix Proteins Female Immunity, Innate Ixodes Lyme Disease - immunology Lyme Disease - microbiology Lyme Disease - pathology Male Mice Mice, Inbred BALB C Mice, Inbred C3H Mice, Knockout Proteoglycans - genetics Proteoglycans - immunology Proteoglycans - physiology |
title | Resistance to Lyme disease in decorin-deficient mice |
url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-03T06%3A02%3A33IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Resistance%20to%20Lyme%20disease%20in%20decorin-deficient%20mice&rft.jtitle=The%20Journal%20of%20clinical%20investigation&rft.au=Brown,%20E%20L&rft.date=2001-04-01&rft.volume=107&rft.issue=7&rft.spage=845&rft.epage=852&rft.pages=845-852&rft.issn=0021-9738&rft_id=info:doi/10.1172/JCI11692&rft_dat=%3Cproquest_pubme%3E18253312%3C/proquest_pubme%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c437t-1ce192c084996aa6dfc360f5d53ab6be4b7f3b6b5b70d130200df01a2d1f9c963%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=18253312&rft_id=info:pmid/11285303&rfr_iscdi=true |