Maternal–fetal transmission of Toxoplasma gondii in interferon-γ deficient pregnant mice
Abstract Toxoplasma gondii infection is generally asymptomatic in immunocompetent persons but can be life-threatening in immunocompromised persons and for fetuses in the case of maternal–fetal transmission. The effect of interferon (IFN)-γ, which plays a crucial role in the protective immunity again...
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| Veröffentlicht in: | Parasitology international 2007-06, Vol.56 (2), p.141-148 |
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| creator | Shiono, Yuko Mun, Hye-Seong He, Na Nakazaki, Yuka Fang, Hao Furuya, Mitsuko Aosai, Fumie Yano, Akihiko |
| description | Abstract Toxoplasma gondii infection is generally asymptomatic in immunocompetent persons but can be life-threatening in immunocompromised persons and for fetuses in the case of maternal–fetal transmission. The effect of interferon (IFN)-γ, which plays a crucial role in the protective immunity against T. gondii infection, on maternal–fetal transmission of T. gondii was analyzed by quantitative competitive polymerase chain reaction targeting T. gondii -specific SAG1 gene. T. gondii loads were obvious in uterus and placenta of wild type (WT) C57BL/6 (B6, susceptible strain) but not BALB/c (resistant strain) pregnant mice. Higher levels of T. gondii were detected in uterus and placenta of IFN-γ knock-out (GKO) B6 and BALB/c than in those of WT mice. Furthermore, T. gondii was detected in fetus of GKO B6 but not GKO BALB/c, WT B6, or WT BALB/c mice. Thus, not only IFN-γ but also genetic susceptibility to T. gondii infection was important for the protective immunity of maternal–fetal transmission of T. gondii to fetus via placenta. T. gondii -infected WT mice displayed a low delivery rate with high IFN-γ production, whereas infected GKO mice did not. Additionally, mean body weight of neonates from T. gondii -infected GKO BALB/c pregnant mice was significantly lower than that of unaborted neonates from WT BALB/c pregnant mice, suggesting the effects of T. gondii infection on intrauterine growth retardation of fetus in pregnant GKO mice. |
| doi_str_mv | 10.1016/j.parint.2007.01.008 |
| format | Article |
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The effect of interferon (IFN)-γ, which plays a crucial role in the protective immunity against T. gondii infection, on maternal–fetal transmission of T. gondii was analyzed by quantitative competitive polymerase chain reaction targeting T. gondii -specific SAG1 gene. T. gondii loads were obvious in uterus and placenta of wild type (WT) C57BL/6 (B6, susceptible strain) but not BALB/c (resistant strain) pregnant mice. Higher levels of T. gondii were detected in uterus and placenta of IFN-γ knock-out (GKO) B6 and BALB/c than in those of WT mice. Furthermore, T. gondii was detected in fetus of GKO B6 but not GKO BALB/c, WT B6, or WT BALB/c mice. Thus, not only IFN-γ but also genetic susceptibility to T. gondii infection was important for the protective immunity of maternal–fetal transmission of T. gondii to fetus via placenta. T. gondii -infected WT mice displayed a low delivery rate with high IFN-γ production, whereas infected GKO mice did not. Additionally, mean body weight of neonates from T. gondii -infected GKO BALB/c pregnant mice was significantly lower than that of unaborted neonates from WT BALB/c pregnant mice, suggesting the effects of T. gondii infection on intrauterine growth retardation of fetus in pregnant GKO mice.</description><identifier>ISSN: 1383-5769</identifier><identifier>EISSN: 1873-0329</identifier><identifier>DOI: 10.1016/j.parint.2007.01.008</identifier><identifier>PMID: 17307382</identifier><language>eng</language><publisher>Netherlands: Elsevier Ireland Ltd</publisher><subject>Animals ; Congenital toxoplasmosis ; Female ; Fetal Growth Retardation - etiology ; Gastroenterology and Hepatology ; Genetic Predisposition to Disease ; Infectious Disease ; Infectious Disease Transmission, Vertical ; Interferon-gamma - deficiency ; Interferon-gamma - genetics ; Interferon-γ ; Intrauterine growth retardation ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Placenta - parasitology ; Placenta Diseases - genetics ; Placenta Diseases - parasitology ; Pregnancy ; Pregnancy Complications, Infectious - genetics ; Pregnancy Complications, Infectious - immunology ; Pregnancy Complications, Infectious - parasitology ; Toxoplasma ; Toxoplasma gondii ; Toxoplasmosis, Animal - genetics ; Toxoplasmosis, Animal - immunology ; Toxoplasmosis, Animal - parasitology ; Toxoplasmosis, Animal - transmission ; Toxoplasmosis, Congenital - etiology ; Toxoplasmosis, Congenital - genetics ; Toxoplasmosis, Congenital - immunology ; Toxoplasmosis, Congenital - parasitology</subject><ispartof>Parasitology international, 2007-06, Vol.56 (2), p.141-148</ispartof><rights>2007</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-fbf982d99fa307eff81f19cc81670420b03a2d52286268c7afb6a45e8386535b3</citedby><cites>FETCH-LOGICAL-c499t-fbf982d99fa307eff81f19cc81670420b03a2d52286268c7afb6a45e8386535b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.parint.2007.01.008$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,777,781,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17307382$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shiono, Yuko</creatorcontrib><creatorcontrib>Mun, Hye-Seong</creatorcontrib><creatorcontrib>He, Na</creatorcontrib><creatorcontrib>Nakazaki, Yuka</creatorcontrib><creatorcontrib>Fang, Hao</creatorcontrib><creatorcontrib>Furuya, Mitsuko</creatorcontrib><creatorcontrib>Aosai, Fumie</creatorcontrib><creatorcontrib>Yano, Akihiko</creatorcontrib><title>Maternal–fetal transmission of Toxoplasma gondii in interferon-γ deficient pregnant mice</title><title>Parasitology international</title><addtitle>Parasitol Int</addtitle><description>Abstract Toxoplasma gondii infection is generally asymptomatic in immunocompetent persons but can be life-threatening in immunocompromised persons and for fetuses in the case of maternal–fetal transmission. The effect of interferon (IFN)-γ, which plays a crucial role in the protective immunity against T. gondii infection, on maternal–fetal transmission of T. gondii was analyzed by quantitative competitive polymerase chain reaction targeting T. gondii -specific SAG1 gene. T. gondii loads were obvious in uterus and placenta of wild type (WT) C57BL/6 (B6, susceptible strain) but not BALB/c (resistant strain) pregnant mice. Higher levels of T. gondii were detected in uterus and placenta of IFN-γ knock-out (GKO) B6 and BALB/c than in those of WT mice. Furthermore, T. gondii was detected in fetus of GKO B6 but not GKO BALB/c, WT B6, or WT BALB/c mice. Thus, not only IFN-γ but also genetic susceptibility to T. gondii infection was important for the protective immunity of maternal–fetal transmission of T. gondii to fetus via placenta. T. gondii -infected WT mice displayed a low delivery rate with high IFN-γ production, whereas infected GKO mice did not. Additionally, mean body weight of neonates from T. gondii -infected GKO BALB/c pregnant mice was significantly lower than that of unaborted neonates from WT BALB/c pregnant mice, suggesting the effects of T. gondii infection on intrauterine growth retardation of fetus in pregnant GKO mice.</description><subject>Animals</subject><subject>Congenital toxoplasmosis</subject><subject>Female</subject><subject>Fetal Growth Retardation - etiology</subject><subject>Gastroenterology and Hepatology</subject><subject>Genetic Predisposition to Disease</subject><subject>Infectious Disease</subject><subject>Infectious Disease Transmission, Vertical</subject><subject>Interferon-gamma - deficiency</subject><subject>Interferon-gamma - genetics</subject><subject>Interferon-γ</subject><subject>Intrauterine growth retardation</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Placenta - parasitology</subject><subject>Placenta Diseases - genetics</subject><subject>Placenta Diseases - parasitology</subject><subject>Pregnancy</subject><subject>Pregnancy Complications, Infectious - genetics</subject><subject>Pregnancy Complications, Infectious - immunology</subject><subject>Pregnancy Complications, Infectious - parasitology</subject><subject>Toxoplasma</subject><subject>Toxoplasma gondii</subject><subject>Toxoplasmosis, Animal - genetics</subject><subject>Toxoplasmosis, Animal - immunology</subject><subject>Toxoplasmosis, Animal - parasitology</subject><subject>Toxoplasmosis, Animal - transmission</subject><subject>Toxoplasmosis, Congenital - etiology</subject><subject>Toxoplasmosis, Congenital - genetics</subject><subject>Toxoplasmosis, Congenital - immunology</subject><subject>Toxoplasmosis, Congenital - parasitology</subject><issn>1383-5769</issn><issn>1873-0329</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkkFu1TAQhiMEoqVwA4SyYpcwtp9je4OEKqBIRV1QViwsxxlXfiR2sPMquuMOHKX36CE4CY7ekyp1U8uSZ_H_v8efp6peE2gJkO7dtp1N8mFpKYBogbQA8kl1TKRgDTCqnpaaSdZw0amj6kXOWwDChSDPqyMiGAgm6XH146tZMAUz_vvz1-FixnpJJuTJ5-xjqKOrL-PvOI8mT6a-imHwvvah7OJymGJo7m7rAZ23HsNSzwmvginF5C2-rJ45M2Z8dThPqu-fPl6enjXnF5-_nH44b-xGqaVxvVOSDko5U7pC5yRxRFkrSSdgQ6EHZujAKZUd7aQVxvWd2XCUTHac8Z6dVG_3uXOKv3aYF13atziOJmDcZS2Acka4elRIlOCSMSjCzV5oU8w5odNz8pNJN5qAXunrrd7T1yt9DUQX-sX25pC_6ycc7k0H3EXwfi_AguPaY9J55WZx8AntoofoH7vhYYAdffDWjD_xBvM27ta_LC_RmWrQ39YJWAcABJQlO_YfZIuvKg</recordid><startdate>20070601</startdate><enddate>20070601</enddate><creator>Shiono, Yuko</creator><creator>Mun, Hye-Seong</creator><creator>He, Na</creator><creator>Nakazaki, Yuka</creator><creator>Fang, Hao</creator><creator>Furuya, Mitsuko</creator><creator>Aosai, Fumie</creator><creator>Yano, Akihiko</creator><general>Elsevier Ireland Ltd</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>7T5</scope><scope>H94</scope><scope>M7N</scope><scope>7X8</scope></search><sort><creationdate>20070601</creationdate><title>Maternal–fetal transmission of Toxoplasma gondii in interferon-γ deficient pregnant mice</title><author>Shiono, Yuko ; Mun, Hye-Seong ; He, Na ; Nakazaki, Yuka ; Fang, Hao ; Furuya, Mitsuko ; Aosai, Fumie ; Yano, Akihiko</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c499t-fbf982d99fa307eff81f19cc81670420b03a2d52286268c7afb6a45e8386535b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Congenital toxoplasmosis</topic><topic>Female</topic><topic>Fetal Growth Retardation - etiology</topic><topic>Gastroenterology and Hepatology</topic><topic>Genetic Predisposition to Disease</topic><topic>Infectious Disease</topic><topic>Infectious Disease Transmission, Vertical</topic><topic>Interferon-gamma - deficiency</topic><topic>Interferon-gamma - genetics</topic><topic>Interferon-γ</topic><topic>Intrauterine growth retardation</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Placenta - parasitology</topic><topic>Placenta Diseases - genetics</topic><topic>Placenta Diseases - parasitology</topic><topic>Pregnancy</topic><topic>Pregnancy Complications, Infectious - genetics</topic><topic>Pregnancy Complications, Infectious - immunology</topic><topic>Pregnancy Complications, Infectious - parasitology</topic><topic>Toxoplasma</topic><topic>Toxoplasma gondii</topic><topic>Toxoplasmosis, Animal - genetics</topic><topic>Toxoplasmosis, Animal - immunology</topic><topic>Toxoplasmosis, Animal - parasitology</topic><topic>Toxoplasmosis, Animal - transmission</topic><topic>Toxoplasmosis, Congenital - etiology</topic><topic>Toxoplasmosis, Congenital - genetics</topic><topic>Toxoplasmosis, Congenital - immunology</topic><topic>Toxoplasmosis, Congenital - parasitology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shiono, Yuko</creatorcontrib><creatorcontrib>Mun, Hye-Seong</creatorcontrib><creatorcontrib>He, Na</creatorcontrib><creatorcontrib>Nakazaki, Yuka</creatorcontrib><creatorcontrib>Fang, Hao</creatorcontrib><creatorcontrib>Furuya, Mitsuko</creatorcontrib><creatorcontrib>Aosai, Fumie</creatorcontrib><creatorcontrib>Yano, Akihiko</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>MEDLINE - Academic</collection><jtitle>Parasitology international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shiono, Yuko</au><au>Mun, Hye-Seong</au><au>He, Na</au><au>Nakazaki, Yuka</au><au>Fang, Hao</au><au>Furuya, Mitsuko</au><au>Aosai, Fumie</au><au>Yano, Akihiko</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Maternal–fetal transmission of Toxoplasma gondii in interferon-γ deficient pregnant mice</atitle><jtitle>Parasitology international</jtitle><addtitle>Parasitol Int</addtitle><date>2007-06-01</date><risdate>2007</risdate><volume>56</volume><issue>2</issue><spage>141</spage><epage>148</epage><pages>141-148</pages><issn>1383-5769</issn><eissn>1873-0329</eissn><abstract>Abstract Toxoplasma gondii infection is generally asymptomatic in immunocompetent persons but can be life-threatening in immunocompromised persons and for fetuses in the case of maternal–fetal transmission. The effect of interferon (IFN)-γ, which plays a crucial role in the protective immunity against T. gondii infection, on maternal–fetal transmission of T. gondii was analyzed by quantitative competitive polymerase chain reaction targeting T. gondii -specific SAG1 gene. T. gondii loads were obvious in uterus and placenta of wild type (WT) C57BL/6 (B6, susceptible strain) but not BALB/c (resistant strain) pregnant mice. Higher levels of T. gondii were detected in uterus and placenta of IFN-γ knock-out (GKO) B6 and BALB/c than in those of WT mice. Furthermore, T. gondii was detected in fetus of GKO B6 but not GKO BALB/c, WT B6, or WT BALB/c mice. Thus, not only IFN-γ but also genetic susceptibility to T. gondii infection was important for the protective immunity of maternal–fetal transmission of T. gondii to fetus via placenta. T. gondii -infected WT mice displayed a low delivery rate with high IFN-γ production, whereas infected GKO mice did not. Additionally, mean body weight of neonates from T. gondii -infected GKO BALB/c pregnant mice was significantly lower than that of unaborted neonates from WT BALB/c pregnant mice, suggesting the effects of T. gondii infection on intrauterine growth retardation of fetus in pregnant GKO mice.</abstract><cop>Netherlands</cop><pub>Elsevier Ireland Ltd</pub><pmid>17307382</pmid><doi>10.1016/j.parint.2007.01.008</doi><tpages>8</tpages></addata></record> |
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| subjects | Animals Congenital toxoplasmosis Female Fetal Growth Retardation - etiology Gastroenterology and Hepatology Genetic Predisposition to Disease Infectious Disease Infectious Disease Transmission, Vertical Interferon-gamma - deficiency Interferon-gamma - genetics Interferon-γ Intrauterine growth retardation Male Mice Mice, Inbred BALB C Mice, Inbred C57BL Mice, Knockout Placenta - parasitology Placenta Diseases - genetics Placenta Diseases - parasitology Pregnancy Pregnancy Complications, Infectious - genetics Pregnancy Complications, Infectious - immunology Pregnancy Complications, Infectious - parasitology Toxoplasma Toxoplasma gondii Toxoplasmosis, Animal - genetics Toxoplasmosis, Animal - immunology Toxoplasmosis, Animal - parasitology Toxoplasmosis, Animal - transmission Toxoplasmosis, Congenital - etiology Toxoplasmosis, Congenital - genetics Toxoplasmosis, Congenital - immunology Toxoplasmosis, Congenital - parasitology |
| title | Maternal–fetal transmission of Toxoplasma gondii in interferon-γ deficient pregnant mice |
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