Rat Strains Differ in Susceptibility to Maternal and Fetal Infection with Mycoplasma pulmonis
Identifieur interne : 001051 ( Main/Exploration ); précédent : 001050; suivant : 001052Rat Strains Differ in Susceptibility to Maternal and Fetal Infection with Mycoplasma pulmonis
Auteurs : Leticia Reyes [États-Unis] ; Micheal Shelton [États-Unis] ; Margaret Riggs [États-Unis] ; Mary B. Brown [États-Unis]Source :
- American Journal of Reproductive Immunology [ 1046-7408 ] ; 2004-03.
English descriptors
- Teeft :
- Adverse pregnancy outcome, Adverse pregnancy outcomes, American journal, Amniotic, Blackwell munksgaard, Cytokine, Dam, Dams inoculated, Fetal, Fetal cultures, Fetal infection, Fetal tissues, Fetal units, Fetus, Genital, Genital mycoplasmosis, Gestation, Gestation time point, Hybridization, Immune mechanisms, Immunology, Infection, Inoculated, Inoculation, Inoculum, Inoculum dose, Intrauterine infection, Intravenous, Intravenous inoculation, Mycoplasma, Mycoplasma pulmonis, Mycoplasmosis, Necropsied, Obstet gynecol, Placenta, Placental, Placental infection, Pregnancy outcome, Pulmonis, Rat, Rats inoculated, Reproductive, Reproductive immunology, Reyes, Sample size, Standard deviation, Strain susceptibility, Susceptibility, Time point, Treatment group, Ureaplasma urealyticum.
Abstract
Problem: Vaginally infected Sprague–Dawley (SD) rats are more susceptible to adverse pregnancy outcomes than Wistar (WIS) rats. We postulated that SD rats have enhanced hematogenous spread of Mycoplasma pulmonis to fetal tissues. Method of study: WIS and SD dams were infected intravenously with 107, 106, and 105 colony‐forming units of M. pulmonis at gestation day 14. Dams and six randomly selected fetuses were cultured at days 15, 16, 17, and 18 of gestation. Results: In the high‐dose group, 100% of fetuses were colonized regardless of rat strain. Significantly higher numbers of M. pulmonis were isolated from placenta (low dose, P < 0.0001; medium dose, P < 0.024; high dose, P < 0.0001), amniotic fluid (low dose, P < 0.003; medium dose, P < 0.017), and fetuses (low dose, P < 0.0011) of SD rats. Spread of M. pulmonis to the amniotic fluid and fetus occurred 1 day earlier in SD rats. Conclusions: The difference in susceptibility between the two rat strains cannot be explained by hematogenous spread alone. The relative resistance to adverse pregnancy outcomes in WIS rats may be a function of a more robust innate immune system. These rat strains may represent an animal model to address host resistance factors to intrauterine infection.
Url:
DOI: 10.1111/j.1600-0897.2004.00144.x
Affiliations:
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Brown</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Floride</region></placeName><wicri:cityArea>Department of Pathobiology, College of Veterinary Medicine, University of Florida, Gainesville</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">American Journal of Reproductive Immunology</title><title level="j" type="alt">AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY</title><idno type="ISSN">1046-7408</idno><idno type="eISSN">1600-0897</idno><imprint><biblScope unit="vol">51</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="211">211</biblScope><biblScope unit="page" to="219">219</biblScope><biblScope unit="page-count">9</biblScope><publisher>Blackwell Publishing</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2004-03">2004-03</date></imprint><idno type="ISSN">1046-7408</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1046-7408</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Adverse pregnancy outcome</term><term>Adverse pregnancy outcomes</term><term>American journal</term><term>Amniotic</term><term>Blackwell munksgaard</term><term>Cytokine</term><term>Dam</term><term>Dams inoculated</term><term>Fetal</term><term>Fetal cultures</term><term>Fetal infection</term><term>Fetal tissues</term><term>Fetal units</term><term>Fetus</term><term>Genital</term><term>Genital mycoplasmosis</term><term>Gestation</term><term>Gestation time point</term><term>Hybridization</term><term>Immune mechanisms</term><term>Immunology</term><term>Infection</term><term>Inoculated</term><term>Inoculation</term><term>Inoculum</term><term>Inoculum dose</term><term>Intrauterine infection</term><term>Intravenous</term><term>Intravenous inoculation</term><term>Mycoplasma</term><term>Mycoplasma pulmonis</term><term>Mycoplasmosis</term><term>Necropsied</term><term>Obstet gynecol</term><term>Placenta</term><term>Placental</term><term>Placental infection</term><term>Pregnancy outcome</term><term>Pulmonis</term><term>Rat</term><term>Rats inoculated</term><term>Reproductive</term><term>Reproductive immunology</term><term>Reyes</term><term>Sample size</term><term>Standard deviation</term><term>Strain susceptibility</term><term>Susceptibility</term><term>Time point</term><term>Treatment group</term><term>Ureaplasma urealyticum</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Problem: Vaginally infected Sprague–Dawley (SD) rats are more susceptible to adverse pregnancy outcomes than Wistar (WIS) rats. We postulated that SD rats have enhanced hematogenous spread of Mycoplasma pulmonis to fetal tissues. Method of study: WIS and SD dams were infected intravenously with 107, 106, and 105 colony‐forming units of M. pulmonis at gestation day 14. Dams and six randomly selected fetuses were cultured at days 15, 16, 17, and 18 of gestation. Results: In the high‐dose group, 100% of fetuses were colonized regardless of rat strain. Significantly higher numbers of M. pulmonis were isolated from placenta (low dose, P < 0.0001; medium dose, P < 0.024; high dose, P < 0.0001), amniotic fluid (low dose, P < 0.003; medium dose, P < 0.017), and fetuses (low dose, P < 0.0011) of SD rats. Spread of M. pulmonis to the amniotic fluid and fetus occurred 1 day earlier in SD rats. Conclusions: The difference in susceptibility between the two rat strains cannot be explained by hematogenous spread alone. The relative resistance to adverse pregnancy outcomes in WIS rats may be a function of a more robust innate immune system. These rat strains may represent an animal model to address host resistance factors to intrauterine infection.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Floride</li><li>Maryland</li></region></list><tree><country name="États-Unis"><region name="Floride"><name sortKey="Reyes, Leticia" sort="Reyes, Leticia" uniqKey="Reyes L" first="Leticia" last="Reyes">Leticia Reyes</name></region><name sortKey="Brown, Mary B" sort="Brown, Mary B" uniqKey="Brown M" first="Mary B." last="Brown">Mary B. Brown</name><name sortKey="Riggs, Margaret" sort="Riggs, Margaret" uniqKey="Riggs M" first="Margaret" last="Riggs">Margaret Riggs</name><name sortKey="Shelton, Micheal" sort="Shelton, Micheal" uniqKey="Shelton M" first="Micheal" last="Shelton">Micheal Shelton</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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