Pathogenesis of Babesia caballi infection in experimental horses
The present study was designed to investigate the role of cytokines in the pathogenesis of Babesia caballi in experimentally infected horses. The expression of cytokine mRNA was determined by using reverse transcription-polymerase chain reaction in two B. caballi-infected horses for 2 weeks after th...
Gespeichert in:
| Veröffentlicht in: | Journal of Veterinary Medical Science 1998, Vol.60(10), pp.1127-1132 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1132 |
|---|---|
| container_issue | 10 |
| container_start_page | 1127 |
| container_title | Journal of Veterinary Medical Science |
| container_volume | 60 |
| creator | Hanafusa, Y. (Hokkaido Univ., Sapporo (Japan)) Cho, K.O Kanemaru, T Wada, R Sugimoto, C Onuma, M |
| description | The present study was designed to investigate the role of cytokines in the pathogenesis of Babesia caballi in experimentally infected horses. The expression of cytokine mRNA was determined by using reverse transcription-polymerase chain reaction in two B. caballi-infected horses for 2 weeks after the infection. In one horse, there was up-regulation of interferon-gamma, tumor necrosis factor-alpha (TNF-α) and interleukin-2 mRNAs, while in the second horse, expression of only TNF-α mRNA was up-regulated. No change was observed in interleukin-4 mRNA in both of the horses. To know the relation between nitric oxide (NO) production and pathogenesis, NO production was assayed in three dexamethasone treated-B. caballi-infected horses. Production of NO in all 3 horses increased significantly before death, although the parasitemia level remained very low. Treatment with NO inhibitor resulted in the suppression of NO production and increased parasitemia level in a horse, which died of the infection. The pathological examination showed that the main cause of the death was dyspnoea and pulmonary edema. Histopathologically, diffuse global mesangial proliferative glomerulonephritis was also observed. These results suggested that NO may be a critical effector molecule of immune defense against parasite. TNF-α and NO might be contributing to the pathogenesis in B. caballi infection. |
| doi_str_mv | 10.1292/jvms.60.1127 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_70067804</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>20711963</sourcerecordid><originalsourceid>FETCH-LOGICAL-c657t-e1c84fdc84ab3ad8614ba97911843fcc455cf3719ee6fc8af1baa5945a272e953</originalsourceid><addsrcrecordid>eNqFkM9r2zAUx8VYabN0t14LhkFPc6tny5J16xb2oyXQHrazeFaeEgfHSiV7rP99FRJS6KWXJz2-H75CH8YugF9DoYub9b9NvJZpgUJ9YBMohcqVKPVHNuEaZK6Kip-xTzGuOS9ASH3KTnUNWkk1YbePOKz8knqKbcy8y75jk66YWWyw69qs7R3ZofV9umX0f0uh3VA_YJetfIgUz9mJwy7S58M5ZX9__vgz-53PH37dzb7NcysrNeQEthZukQY2JS5qCaJBrTRALUpnragq60oFmkg6W6ODBrHSosJCFaSrcsqu9r3b4J9GioPZtNFS12FPfoxGcS5VzcW7YMEVgJZlAr-8Add-DH36hEmWaqkUr3Wivu4pG3yMgZzZJgMYng1ws_Nvdv6NTEvyn_DLQ-nYbGhxhA_CUz7b5-s44JKOOYahtR29lvHD3LUeU7vCYKh_fcWhN7gMbTT3j6C15hwgOXgBbFuhRw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1468677089</pqid></control><display><type>article</type><title>Pathogenesis of Babesia caballi infection in experimental horses</title><source>MEDLINE</source><source>J-STAGE (Japan Science & Technology Information Aggregator, Electronic) Freely Available Titles - Japanese</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>Hanafusa, Y. (Hokkaido Univ., Sapporo (Japan)) ; Cho, K.O ; Kanemaru, T ; Wada, R ; Sugimoto, C ; Onuma, M</creator><creatorcontrib>Hanafusa, Y. (Hokkaido Univ., Sapporo (Japan)) ; Cho, K.O ; Kanemaru, T ; Wada, R ; Sugimoto, C ; Onuma, M</creatorcontrib><description>The present study was designed to investigate the role of cytokines in the pathogenesis of Babesia caballi in experimentally infected horses. The expression of cytokine mRNA was determined by using reverse transcription-polymerase chain reaction in two B. caballi-infected horses for 2 weeks after the infection. In one horse, there was up-regulation of interferon-gamma, tumor necrosis factor-alpha (TNF-α) and interleukin-2 mRNAs, while in the second horse, expression of only TNF-α mRNA was up-regulated. No change was observed in interleukin-4 mRNA in both of the horses. To know the relation between nitric oxide (NO) production and pathogenesis, NO production was assayed in three dexamethasone treated-B. caballi-infected horses. Production of NO in all 3 horses increased significantly before death, although the parasitemia level remained very low. Treatment with NO inhibitor resulted in the suppression of NO production and increased parasitemia level in a horse, which died of the infection. The pathological examination showed that the main cause of the death was dyspnoea and pulmonary edema. Histopathologically, diffuse global mesangial proliferative glomerulonephritis was also observed. These results suggested that NO may be a critical effector molecule of immune defense against parasite. TNF-α and NO might be contributing to the pathogenesis in B. caballi infection.</description><identifier>ISSN: 0916-7250</identifier><identifier>EISSN: 1347-7439</identifier><identifier>DOI: 10.1292/jvms.60.1127</identifier><identifier>PMID: 9819767</identifier><language>eng</language><publisher>Japan: JAPANESE SOCIETY OF VETERINARY SCIENCE</publisher><subject>Animals ; Babesia - genetics ; Babesia - pathogenicity ; Babesia caballi ; BABESIA EQUI ; Babesiosis - complications ; Babesiosis - immunology ; Babesiosis - parasitology ; CABALLOS ; CHEVAL ; CITOQUINAS ; CYTOKINE ; CYTOKINES ; Cytokines - biosynthesis ; EXPERIMENTAL INFECTION ; Horse Diseases - immunology ; Horse Diseases - parasitology ; HORSES ; INFECCION EXPERIMENTAL ; INFECTION EXPERIMENTALE ; nitric oxide ; Nitric Oxide - biosynthesis ; PATHOGENESE ; PATHOGENESIS ; PATOGENESIS ; Pulmonary Edema - etiology ; Pulmonary Edema - mortality ; Pulmonary Edema - veterinary ; RNA, Messenger - metabolism ; Tumor Necrosis Factor-alpha - genetics ; Up-Regulation</subject><ispartof>Journal of Veterinary Medical Science, 1998, Vol.60(10), pp.1127-1132</ispartof><rights>1998 by the Japanese Society of Veterinary Science</rights><rights>Copyright Japan Science and Technology Agency 1998</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c657t-e1c84fdc84ab3ad8614ba97911843fcc455cf3719ee6fc8af1baa5945a272e953</citedby><cites>FETCH-LOGICAL-c657t-e1c84fdc84ab3ad8614ba97911843fcc455cf3719ee6fc8af1baa5945a272e953</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1877,4010,27900,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9819767$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hanafusa, Y. (Hokkaido Univ., Sapporo (Japan))</creatorcontrib><creatorcontrib>Cho, K.O</creatorcontrib><creatorcontrib>Kanemaru, T</creatorcontrib><creatorcontrib>Wada, R</creatorcontrib><creatorcontrib>Sugimoto, C</creatorcontrib><creatorcontrib>Onuma, M</creatorcontrib><title>Pathogenesis of Babesia caballi infection in experimental horses</title><title>Journal of Veterinary Medical Science</title><addtitle>J. Vet. Med. Sci.</addtitle><description>The present study was designed to investigate the role of cytokines in the pathogenesis of Babesia caballi in experimentally infected horses. The expression of cytokine mRNA was determined by using reverse transcription-polymerase chain reaction in two B. caballi-infected horses for 2 weeks after the infection. In one horse, there was up-regulation of interferon-gamma, tumor necrosis factor-alpha (TNF-α) and interleukin-2 mRNAs, while in the second horse, expression of only TNF-α mRNA was up-regulated. No change was observed in interleukin-4 mRNA in both of the horses. To know the relation between nitric oxide (NO) production and pathogenesis, NO production was assayed in three dexamethasone treated-B. caballi-infected horses. Production of NO in all 3 horses increased significantly before death, although the parasitemia level remained very low. Treatment with NO inhibitor resulted in the suppression of NO production and increased parasitemia level in a horse, which died of the infection. The pathological examination showed that the main cause of the death was dyspnoea and pulmonary edema. Histopathologically, diffuse global mesangial proliferative glomerulonephritis was also observed. These results suggested that NO may be a critical effector molecule of immune defense against parasite. TNF-α and NO might be contributing to the pathogenesis in B. caballi infection.</description><subject>Animals</subject><subject>Babesia - genetics</subject><subject>Babesia - pathogenicity</subject><subject>Babesia caballi</subject><subject>BABESIA EQUI</subject><subject>Babesiosis - complications</subject><subject>Babesiosis - immunology</subject><subject>Babesiosis - parasitology</subject><subject>CABALLOS</subject><subject>CHEVAL</subject><subject>CITOQUINAS</subject><subject>CYTOKINE</subject><subject>CYTOKINES</subject><subject>Cytokines - biosynthesis</subject><subject>EXPERIMENTAL INFECTION</subject><subject>Horse Diseases - immunology</subject><subject>Horse Diseases - parasitology</subject><subject>HORSES</subject><subject>INFECCION EXPERIMENTAL</subject><subject>INFECTION EXPERIMENTALE</subject><subject>nitric oxide</subject><subject>Nitric Oxide - biosynthesis</subject><subject>PATHOGENESE</subject><subject>PATHOGENESIS</subject><subject>PATOGENESIS</subject><subject>Pulmonary Edema - etiology</subject><subject>Pulmonary Edema - mortality</subject><subject>Pulmonary Edema - veterinary</subject><subject>RNA, Messenger - metabolism</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Up-Regulation</subject><issn>0916-7250</issn><issn>1347-7439</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkM9r2zAUx8VYabN0t14LhkFPc6tny5J16xb2oyXQHrazeFaeEgfHSiV7rP99FRJS6KWXJz2-H75CH8YugF9DoYub9b9NvJZpgUJ9YBMohcqVKPVHNuEaZK6Kip-xTzGuOS9ASH3KTnUNWkk1YbePOKz8knqKbcy8y75jk66YWWyw69qs7R3ZofV9umX0f0uh3VA_YJetfIgUz9mJwy7S58M5ZX9__vgz-53PH37dzb7NcysrNeQEthZukQY2JS5qCaJBrTRALUpnragq60oFmkg6W6ODBrHSosJCFaSrcsqu9r3b4J9GioPZtNFS12FPfoxGcS5VzcW7YMEVgJZlAr-8Add-DH36hEmWaqkUr3Wivu4pG3yMgZzZJgMYng1ws_Nvdv6NTEvyn_DLQ-nYbGhxhA_CUz7b5-s44JKOOYahtR29lvHD3LUeU7vCYKh_fcWhN7gMbTT3j6C15hwgOXgBbFuhRw</recordid><startdate>1998</startdate><enddate>1998</enddate><creator>Hanafusa, Y. (Hokkaido Univ., Sapporo (Japan))</creator><creator>Cho, K.O</creator><creator>Kanemaru, T</creator><creator>Wada, R</creator><creator>Sugimoto, C</creator><creator>Onuma, M</creator><general>JAPANESE SOCIETY OF VETERINARY SCIENCE</general><general>Japan Science and Technology Agency</general><scope>FBQ</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>7QR</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>1998</creationdate><title>Pathogenesis of Babesia caballi infection in experimental horses</title><author>Hanafusa, Y. (Hokkaido Univ., Sapporo (Japan)) ; Cho, K.O ; Kanemaru, T ; Wada, R ; Sugimoto, C ; Onuma, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c657t-e1c84fdc84ab3ad8614ba97911843fcc455cf3719ee6fc8af1baa5945a272e953</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Animals</topic><topic>Babesia - genetics</topic><topic>Babesia - pathogenicity</topic><topic>Babesia caballi</topic><topic>BABESIA EQUI</topic><topic>Babesiosis - complications</topic><topic>Babesiosis - immunology</topic><topic>Babesiosis - parasitology</topic><topic>CABALLOS</topic><topic>CHEVAL</topic><topic>CITOQUINAS</topic><topic>CYTOKINE</topic><topic>CYTOKINES</topic><topic>Cytokines - biosynthesis</topic><topic>EXPERIMENTAL INFECTION</topic><topic>Horse Diseases - immunology</topic><topic>Horse Diseases - parasitology</topic><topic>HORSES</topic><topic>INFECCION EXPERIMENTAL</topic><topic>INFECTION EXPERIMENTALE</topic><topic>nitric oxide</topic><topic>Nitric Oxide - biosynthesis</topic><topic>PATHOGENESE</topic><topic>PATHOGENESIS</topic><topic>PATOGENESIS</topic><topic>Pulmonary Edema - etiology</topic><topic>Pulmonary Edema - mortality</topic><topic>Pulmonary Edema - veterinary</topic><topic>RNA, Messenger - metabolism</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hanafusa, Y. (Hokkaido Univ., Sapporo (Japan))</creatorcontrib><creatorcontrib>Cho, K.O</creatorcontrib><creatorcontrib>Kanemaru, T</creatorcontrib><creatorcontrib>Wada, R</creatorcontrib><creatorcontrib>Sugimoto, C</creatorcontrib><creatorcontrib>Onuma, M</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Chemoreception Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of Veterinary Medical Science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hanafusa, Y. (Hokkaido Univ., Sapporo (Japan))</au><au>Cho, K.O</au><au>Kanemaru, T</au><au>Wada, R</au><au>Sugimoto, C</au><au>Onuma, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pathogenesis of Babesia caballi infection in experimental horses</atitle><jtitle>Journal of Veterinary Medical Science</jtitle><addtitle>J. Vet. Med. Sci.</addtitle><date>1998</date><risdate>1998</risdate><volume>60</volume><issue>10</issue><spage>1127</spage><epage>1132</epage><pages>1127-1132</pages><issn>0916-7250</issn><eissn>1347-7439</eissn><abstract>The present study was designed to investigate the role of cytokines in the pathogenesis of Babesia caballi in experimentally infected horses. The expression of cytokine mRNA was determined by using reverse transcription-polymerase chain reaction in two B. caballi-infected horses for 2 weeks after the infection. In one horse, there was up-regulation of interferon-gamma, tumor necrosis factor-alpha (TNF-α) and interleukin-2 mRNAs, while in the second horse, expression of only TNF-α mRNA was up-regulated. No change was observed in interleukin-4 mRNA in both of the horses. To know the relation between nitric oxide (NO) production and pathogenesis, NO production was assayed in three dexamethasone treated-B. caballi-infected horses. Production of NO in all 3 horses increased significantly before death, although the parasitemia level remained very low. Treatment with NO inhibitor resulted in the suppression of NO production and increased parasitemia level in a horse, which died of the infection. The pathological examination showed that the main cause of the death was dyspnoea and pulmonary edema. Histopathologically, diffuse global mesangial proliferative glomerulonephritis was also observed. These results suggested that NO may be a critical effector molecule of immune defense against parasite. TNF-α and NO might be contributing to the pathogenesis in B. caballi infection.</abstract><cop>Japan</cop><pub>JAPANESE SOCIETY OF VETERINARY SCIENCE</pub><pmid>9819767</pmid><doi>10.1292/jvms.60.1127</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0916-7250 |
| ispartof | Journal of Veterinary Medical Science, 1998, Vol.60(10), pp.1127-1132 |
| issn | 0916-7250 1347-7439 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_70067804 |
| source | MEDLINE; J-STAGE (Japan Science & Technology Information Aggregator, Electronic) Freely Available Titles - Japanese; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Animals Babesia - genetics Babesia - pathogenicity Babesia caballi BABESIA EQUI Babesiosis - complications Babesiosis - immunology Babesiosis - parasitology CABALLOS CHEVAL CITOQUINAS CYTOKINE CYTOKINES Cytokines - biosynthesis EXPERIMENTAL INFECTION Horse Diseases - immunology Horse Diseases - parasitology HORSES INFECCION EXPERIMENTAL INFECTION EXPERIMENTALE nitric oxide Nitric Oxide - biosynthesis PATHOGENESE PATHOGENESIS PATOGENESIS Pulmonary Edema - etiology Pulmonary Edema - mortality Pulmonary Edema - veterinary RNA, Messenger - metabolism Tumor Necrosis Factor-alpha - genetics Up-Regulation |
| title | Pathogenesis of Babesia caballi infection in experimental horses |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-15T12%3A44%3A47IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Pathogenesis%20of%20Babesia%20caballi%20infection%20in%20experimental%20horses&rft.jtitle=Journal%20of%20Veterinary%20Medical%20Science&rft.au=Hanafusa,%20Y.%20(Hokkaido%20Univ.,%20Sapporo%20(Japan))&rft.date=1998&rft.volume=60&rft.issue=10&rft.spage=1127&rft.epage=1132&rft.pages=1127-1132&rft.issn=0916-7250&rft.eissn=1347-7439&rft_id=info:doi/10.1292/jvms.60.1127&rft_dat=%3Cproquest_cross%3E20711963%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1468677089&rft_id=info:pmid/9819767&rfr_iscdi=true |