| pubmed-article:2496163 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2496163 | lifeskim:mentions | umls-concept:C0021311 | lld:lifeskim |
| pubmed-article:2496163 | lifeskim:mentions | umls-concept:C0038952 | lld:lifeskim |
| pubmed-article:2496163 | lifeskim:mentions | umls-concept:C0301872 | lld:lifeskim |
| pubmed-article:2496163 | lifeskim:mentions | umls-concept:C0332281 | lld:lifeskim |
| pubmed-article:2496163 | lifeskim:mentions | umls-concept:C0040557 | lld:lifeskim |
| pubmed-article:2496163 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:2496163 | pubmed:dateCreated | 1989-5-31 | lld:pubmed |
| pubmed-article:2496163 | pubmed:abstractText | After peroral infection with cysts of Toxoplasma gondii, C57BL/6 mice died and A/J mice survived. To better understand the reasons for this difference in survival, host defenses during acute infection were studied: initial portal of entry of T. gondii contributed to susceptibility as more C57BL/6 mice survived after i.p. than peroral infection (p less than 0.001). Susceptible (C57BL/6) mice had more necrosis and inflammation in their brains, livers, and mesenteric lymph nodes than resistant (A/J) mice. Susceptible mice had less IgM antibody to T. gondii (p less than 0.0005) than resistant mice 7 days after infection, but amounts of IgG antibody to T. gondii were similar. Infection reduced percentages of spleen cells with the Lyt-2+ phenotype in susceptible (p less than 0.02) but not resistant mice; infection decreased percentages of spleen cells with the L3T4+ phenotype similarly in both strains of mice. Spleen cells from infected susceptible mice had greater depression in their blastogenic response to Con A (p less than 0.05) and produced significantly more IFN-gamma in culture with (p = 0.009) or without (p less than 0.05) Toxoplasma Ag than spleen cells from infected resistant mice. Infection increased serum levels of IFN-gamma substantially in susceptible but not resistant mice. Lymphocyte IL-2 production was similar in both groups of mice. Peritoneal macrophages from both strains of mice became activated to inhibit or kill T. gondii by 7 days after infection, but Kupffer cells became activated only in susceptible mice. These results indicate that increased resistance to peroral Toxoplasma infection is likely to be mediated by a number of immune responses acting together. They suggest that increased susceptibility may result from inadequately regulated inflammatory responses that increase tissue destruction. | lld:pubmed |
| pubmed-article:2496163 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2496163 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2496163 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2496163 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:2496163 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2496163 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2496163 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2496163 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2496163 | pubmed:month | May | lld:pubmed |
| pubmed-article:2496163 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:2496163 | pubmed:author | pubmed-author:BrownCC | lld:pubmed |
| pubmed-article:2496163 | pubmed:author | pubmed-author:McLeodRR | lld:pubmed |
| pubmed-article:2496163 | pubmed:author | pubmed-author:FiliceGG | lld:pubmed |
| pubmed-article:2496163 | pubmed:author | pubmed-author:MackDD | lld:pubmed |
| pubmed-article:2496163 | pubmed:author | pubmed-author:SpitalnyGG | lld:pubmed |
| pubmed-article:2496163 | pubmed:author | pubmed-author:EisenhauerPP | lld:pubmed |
| pubmed-article:2496163 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2496163 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:2496163 | pubmed:volume | 142 | lld:pubmed |
| pubmed-article:2496163 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2496163 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2496163 | pubmed:pagination | 3247-55 | lld:pubmed |
| pubmed-article:2496163 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:2496163 | pubmed:year | 1989 | lld:pubmed |
| pubmed-article:2496163 | pubmed:articleTitle | Immune responses associated with early survival after peroral infection with Toxoplasma gondii. | lld:pubmed |
| pubmed-article:2496163 | pubmed:affiliation | Department of Medicine, Michael Reese Medical Center, Chicago, IL 60616. | lld:pubmed |
| pubmed-article:2496163 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2496163 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:2496163 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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