Loading…
Attenuated host resistance against Mycobacterium bovis BCG infection in mice lacking osteopontin
Expression of the cytokine osteopontin (OPN) is elevated in granulomas caused by Mycobacterium tuberculosis. We tested the hypothesis that OPN contributes to host protection in a mouse model of mycobacterial infection. When infected with Mycobacterium bovis BCG, mice lacking a functional OPN gene ha...
Saved in:
Published in: | Infection and immunity 1999-08, Vol.67 (8), p.4223-4230 |
---|---|
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-c422t-fea5573e79d5d17e2b2f6ec8c7462ab8be7f88c74a9976ebd64e60582920c5a63 |
---|---|
cites | cdi_FETCH-LOGICAL-c422t-fea5573e79d5d17e2b2f6ec8c7462ab8be7f88c74a9976ebd64e60582920c5a63 |
container_end_page | 4230 |
container_issue | 8 |
container_start_page | 4223 |
container_title | Infection and immunity |
container_volume | 67 |
creator | NAU, G. J LIAW, L CHUPP, G. L BERMAN, J. S HOGAN, B. L. M YOUNG, R. A |
description | Expression of the cytokine osteopontin (OPN) is elevated in granulomas caused by Mycobacterium tuberculosis. We tested the hypothesis that OPN contributes to host protection in a mouse model of mycobacterial infection. When infected with Mycobacterium bovis BCG, mice lacking a functional OPN gene had more severe infections characterized by heavier bacterial loads and a delayed clearance of the bacteria. The OPN-null mice had greater granuloma burdens consistent with the elevated bacterial load. The ability of osteopontin to facilitate the clearance of mycobacteria was most pronounced early after infection and appeared to be independent of known mediators of resistance to infection by mycobacteria: antigen-specific T-cell immunity, gamma interferon production, and nitric oxide production. BCG grew more rapidly in macrophages derived from OPN-null mice than in those from wild-type mice, demonstrating that the null phenotype was due to an intrinsic macrophage defect. These results indicate that osteopontin augments the host response against a mycobacterial infection and that it acts independently from other antimycobacterial resistance mechanisms. |
doi_str_mv | 10.1128/IAI.67.8.4223-4230.1999 |
format | article |
fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_96728</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>17311197</sourcerecordid><originalsourceid>FETCH-LOGICAL-c422t-fea5573e79d5d17e2b2f6ec8c7462ab8be7f88c74a9976ebd64e60582920c5a63</originalsourceid><addsrcrecordid>eNqFkU1v1DAQhi1ERbeFvwA5IG5ZbMfxh8RlWUFZqVUvcDaOM9kaEnuxnUr993W0K1pOnOwZP-_IowehdwSvCaHy426zW3OxlmtGaVMz2pS-UuoFWhGsZN22lL5EK4yJqlXLxTm6SOlXKRlj8hU6J5gRQVS7Qj83OYOfTYa-ugspVxGSS9l4C5XZG-dL6-bBhs7YDNHNU9WFe5eqz9uryvkBbHbBl1s1uZIYjf3t_L4qgyAcgs_Ov0ZngxkTvDmdl-jH1y_ft9_q69ur3XZzXduyQq4HMG0rGhCqb3sigHZ04GClFYxT08kOxCCXyiglOHQ9Z8BxK6mi2LaGN5fo03HuYe4m6C34HM2oD9FNJj7oYJz-98W7O70P91pxQWWJfzjFY_gzQ8p6csnCOBoPYU6aK4UVk-q_IBENIUSJAoojaGNIKcLw9y8E60WiLhI1F1rqRaJeJOpFYkm-fb7Ks9zRWgHenwCTrBmHWHS59MTRRhEum0eBZag7</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>17311197</pqid></control><display><type>article</type><title>Attenuated host resistance against Mycobacterium bovis BCG infection in mice lacking osteopontin</title><source>American Society for Microbiology Journals</source><source>PubMed Central</source><creator>NAU, G. J ; LIAW, L ; CHUPP, G. L ; BERMAN, J. S ; HOGAN, B. L. M ; YOUNG, R. A</creator><contributor>Kaufmann, S. H. E.</contributor><creatorcontrib>NAU, G. J ; LIAW, L ; CHUPP, G. L ; BERMAN, J. S ; HOGAN, B. L. M ; YOUNG, R. A ; Kaufmann, S. H. E.</creatorcontrib><description>Expression of the cytokine osteopontin (OPN) is elevated in granulomas caused by Mycobacterium tuberculosis. We tested the hypothesis that OPN contributes to host protection in a mouse model of mycobacterial infection. When infected with Mycobacterium bovis BCG, mice lacking a functional OPN gene had more severe infections characterized by heavier bacterial loads and a delayed clearance of the bacteria. The OPN-null mice had greater granuloma burdens consistent with the elevated bacterial load. The ability of osteopontin to facilitate the clearance of mycobacteria was most pronounced early after infection and appeared to be independent of known mediators of resistance to infection by mycobacteria: antigen-specific T-cell immunity, gamma interferon production, and nitric oxide production. BCG grew more rapidly in macrophages derived from OPN-null mice than in those from wild-type mice, demonstrating that the null phenotype was due to an intrinsic macrophage defect. These results indicate that osteopontin augments the host response against a mycobacterial infection and that it acts independently from other antimycobacterial resistance mechanisms.</description><identifier>ISSN: 0019-9567</identifier><identifier>EISSN: 1098-5522</identifier><identifier>DOI: 10.1128/IAI.67.8.4223-4230.1999</identifier><identifier>PMID: 10417195</identifier><identifier>CODEN: INFIBR</identifier><language>eng</language><publisher>Washington, DC: American Society for Microbiology</publisher><subject>Animals ; Bacterial diseases ; Bacteriology ; Biological and medical sciences ; Cytokines - physiology ; Experimental bacterial diseases and models ; Fundamental and applied biological sciences. Psychology ; Granuloma - etiology ; Host Response and Inflammation ; Hyaluronan Receptors - physiology ; Infectious diseases ; Interferon-gamma - biosynthesis ; Macrophages - physiology ; Medical sciences ; Mice ; Microbiology ; Mycobacterium bovis ; Nitric Oxide - metabolism ; Osteopontin ; Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains ; Sialoglycoproteins - genetics ; Sialoglycoproteins - physiology ; Tuberculosis - immunology ; Uracil - metabolism</subject><ispartof>Infection and immunity, 1999-08, Vol.67 (8), p.4223-4230</ispartof><rights>2000 INIST-CNRS</rights><rights>Copyright © 1999, American Society for Microbiology 1999</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c422t-fea5573e79d5d17e2b2f6ec8c7462ab8be7f88c74a9976ebd64e60582920c5a63</citedby><cites>FETCH-LOGICAL-c422t-fea5573e79d5d17e2b2f6ec8c7462ab8be7f88c74a9976ebd64e60582920c5a63</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/PMC96728/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC96728/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,3188,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1239168$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10417195$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Kaufmann, S. H. E.</contributor><creatorcontrib>NAU, G. J</creatorcontrib><creatorcontrib>LIAW, L</creatorcontrib><creatorcontrib>CHUPP, G. L</creatorcontrib><creatorcontrib>BERMAN, J. S</creatorcontrib><creatorcontrib>HOGAN, B. L. M</creatorcontrib><creatorcontrib>YOUNG, R. A</creatorcontrib><title>Attenuated host resistance against Mycobacterium bovis BCG infection in mice lacking osteopontin</title><title>Infection and immunity</title><addtitle>Infect Immun</addtitle><description>Expression of the cytokine osteopontin (OPN) is elevated in granulomas caused by Mycobacterium tuberculosis. We tested the hypothesis that OPN contributes to host protection in a mouse model of mycobacterial infection. When infected with Mycobacterium bovis BCG, mice lacking a functional OPN gene had more severe infections characterized by heavier bacterial loads and a delayed clearance of the bacteria. The OPN-null mice had greater granuloma burdens consistent with the elevated bacterial load. The ability of osteopontin to facilitate the clearance of mycobacteria was most pronounced early after infection and appeared to be independent of known mediators of resistance to infection by mycobacteria: antigen-specific T-cell immunity, gamma interferon production, and nitric oxide production. BCG grew more rapidly in macrophages derived from OPN-null mice than in those from wild-type mice, demonstrating that the null phenotype was due to an intrinsic macrophage defect. These results indicate that osteopontin augments the host response against a mycobacterial infection and that it acts independently from other antimycobacterial resistance mechanisms.</description><subject>Animals</subject><subject>Bacterial diseases</subject><subject>Bacteriology</subject><subject>Biological and medical sciences</subject><subject>Cytokines - physiology</subject><subject>Experimental bacterial diseases and models</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Granuloma - etiology</subject><subject>Host Response and Inflammation</subject><subject>Hyaluronan Receptors - physiology</subject><subject>Infectious diseases</subject><subject>Interferon-gamma - biosynthesis</subject><subject>Macrophages - physiology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Microbiology</subject><subject>Mycobacterium bovis</subject><subject>Nitric Oxide - metabolism</subject><subject>Osteopontin</subject><subject>Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains</subject><subject>Sialoglycoproteins - genetics</subject><subject>Sialoglycoproteins - physiology</subject><subject>Tuberculosis - immunology</subject><subject>Uracil - metabolism</subject><issn>0019-9567</issn><issn>1098-5522</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><recordid>eNqFkU1v1DAQhi1ERbeFvwA5IG5ZbMfxh8RlWUFZqVUvcDaOM9kaEnuxnUr993W0K1pOnOwZP-_IowehdwSvCaHy426zW3OxlmtGaVMz2pS-UuoFWhGsZN22lL5EK4yJqlXLxTm6SOlXKRlj8hU6J5gRQVS7Qj83OYOfTYa-ugspVxGSS9l4C5XZG-dL6-bBhs7YDNHNU9WFe5eqz9uryvkBbHbBl1s1uZIYjf3t_L4qgyAcgs_Ov0ZngxkTvDmdl-jH1y_ft9_q69ur3XZzXduyQq4HMG0rGhCqb3sigHZ04GClFYxT08kOxCCXyiglOHQ9Z8BxK6mi2LaGN5fo03HuYe4m6C34HM2oD9FNJj7oYJz-98W7O70P91pxQWWJfzjFY_gzQ8p6csnCOBoPYU6aK4UVk-q_IBENIUSJAoojaGNIKcLw9y8E60WiLhI1F1rqRaJeJOpFYkm-fb7Ks9zRWgHenwCTrBmHWHS59MTRRhEum0eBZag7</recordid><startdate>19990801</startdate><enddate>19990801</enddate><creator>NAU, G. J</creator><creator>LIAW, L</creator><creator>CHUPP, G. L</creator><creator>BERMAN, J. S</creator><creator>HOGAN, B. L. M</creator><creator>YOUNG, R. A</creator><general>American Society for Microbiology</general><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>7QL</scope><scope>C1K</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19990801</creationdate><title>Attenuated host resistance against Mycobacterium bovis BCG infection in mice lacking osteopontin</title><author>NAU, G. J ; LIAW, L ; CHUPP, G. L ; BERMAN, J. S ; HOGAN, B. L. M ; YOUNG, R. A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c422t-fea5573e79d5d17e2b2f6ec8c7462ab8be7f88c74a9976ebd64e60582920c5a63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Animals</topic><topic>Bacterial diseases</topic><topic>Bacteriology</topic><topic>Biological and medical sciences</topic><topic>Cytokines - physiology</topic><topic>Experimental bacterial diseases and models</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Granuloma - etiology</topic><topic>Host Response and Inflammation</topic><topic>Hyaluronan Receptors - physiology</topic><topic>Infectious diseases</topic><topic>Interferon-gamma - biosynthesis</topic><topic>Macrophages - physiology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Microbiology</topic><topic>Mycobacterium bovis</topic><topic>Nitric Oxide - metabolism</topic><topic>Osteopontin</topic><topic>Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains</topic><topic>Sialoglycoproteins - genetics</topic><topic>Sialoglycoproteins - physiology</topic><topic>Tuberculosis - immunology</topic><topic>Uracil - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>NAU, G. J</creatorcontrib><creatorcontrib>LIAW, L</creatorcontrib><creatorcontrib>CHUPP, G. L</creatorcontrib><creatorcontrib>BERMAN, J. S</creatorcontrib><creatorcontrib>HOGAN, B. L. M</creatorcontrib><creatorcontrib>YOUNG, R. A</creatorcontrib><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>Bacteriology Abstracts (Microbiology B)</collection><collection>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Infection and immunity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>NAU, G. J</au><au>LIAW, L</au><au>CHUPP, G. L</au><au>BERMAN, J. S</au><au>HOGAN, B. L. M</au><au>YOUNG, R. A</au><au>Kaufmann, S. H. E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Attenuated host resistance against Mycobacterium bovis BCG infection in mice lacking osteopontin</atitle><jtitle>Infection and immunity</jtitle><addtitle>Infect Immun</addtitle><date>1999-08-01</date><risdate>1999</risdate><volume>67</volume><issue>8</issue><spage>4223</spage><epage>4230</epage><pages>4223-4230</pages><issn>0019-9567</issn><eissn>1098-5522</eissn><coden>INFIBR</coden><abstract>Expression of the cytokine osteopontin (OPN) is elevated in granulomas caused by Mycobacterium tuberculosis. We tested the hypothesis that OPN contributes to host protection in a mouse model of mycobacterial infection. When infected with Mycobacterium bovis BCG, mice lacking a functional OPN gene had more severe infections characterized by heavier bacterial loads and a delayed clearance of the bacteria. The OPN-null mice had greater granuloma burdens consistent with the elevated bacterial load. The ability of osteopontin to facilitate the clearance of mycobacteria was most pronounced early after infection and appeared to be independent of known mediators of resistance to infection by mycobacteria: antigen-specific T-cell immunity, gamma interferon production, and nitric oxide production. BCG grew more rapidly in macrophages derived from OPN-null mice than in those from wild-type mice, demonstrating that the null phenotype was due to an intrinsic macrophage defect. These results indicate that osteopontin augments the host response against a mycobacterial infection and that it acts independently from other antimycobacterial resistance mechanisms.</abstract><cop>Washington, DC</cop><pub>American Society for Microbiology</pub><pmid>10417195</pmid><doi>10.1128/IAI.67.8.4223-4230.1999</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0019-9567 |
ispartof | Infection and immunity, 1999-08, Vol.67 (8), p.4223-4230 |
issn | 0019-9567 1098-5522 |
language | eng |
recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_96728 |
source | American Society for Microbiology Journals; PubMed Central |
subjects | Animals Bacterial diseases Bacteriology Biological and medical sciences Cytokines - physiology Experimental bacterial diseases and models Fundamental and applied biological sciences. Psychology Granuloma - etiology Host Response and Inflammation Hyaluronan Receptors - physiology Infectious diseases Interferon-gamma - biosynthesis Macrophages - physiology Medical sciences Mice Microbiology Mycobacterium bovis Nitric Oxide - metabolism Osteopontin Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains Sialoglycoproteins - genetics Sialoglycoproteins - physiology Tuberculosis - immunology Uracil - metabolism |
title | Attenuated host resistance against Mycobacterium bovis BCG infection in mice lacking osteopontin |
url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-25T14%3A40%3A37IST&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=Attenuated%20host%20resistance%20against%20Mycobacterium%20bovis%20BCG%20infection%20in%20mice%20lacking%20osteopontin&rft.jtitle=Infection%20and%20immunity&rft.au=NAU,%20G.%20J&rft.date=1999-08-01&rft.volume=67&rft.issue=8&rft.spage=4223&rft.epage=4230&rft.pages=4223-4230&rft.issn=0019-9567&rft.eissn=1098-5522&rft.coden=INFIBR&rft_id=info:doi/10.1128/IAI.67.8.4223-4230.1999&rft_dat=%3Cproquest_pubme%3E17311197%3C/proquest_pubme%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c422t-fea5573e79d5d17e2b2f6ec8c7462ab8be7f88c74a9976ebd64e60582920c5a63%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=17311197&rft_id=info:pmid/10417195&rfr_iscdi=true |