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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
9
|
| pubmed:dateCreated |
1989-5-31
|
| 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.
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| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
May
|
| pubmed:issn |
0022-1767
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
1
|
| pubmed:volume |
142
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
3247-55
|
| pubmed:dateRevised |
2008-11-21
|
| pubmed:meshHeading |
pubmed-meshheading:2496163-Animals,
pubmed-meshheading:2496163-Antibodies, Protozoan,
pubmed-meshheading:2496163-Antigens, Protozoan,
pubmed-meshheading:2496163-Brain Diseases,
pubmed-meshheading:2496163-Cysts,
pubmed-meshheading:2496163-Disease Susceptibility,
pubmed-meshheading:2496163-Female,
pubmed-meshheading:2496163-Immunity, Innate,
pubmed-meshheading:2496163-Interferon-gamma,
pubmed-meshheading:2496163-Kupffer Cells,
pubmed-meshheading:2496163-Liver Diseases, Parasitic,
pubmed-meshheading:2496163-Lymphocyte Activation,
pubmed-meshheading:2496163-Macrophage Activation,
pubmed-meshheading:2496163-Male,
pubmed-meshheading:2496163-Mice,
pubmed-meshheading:2496163-Mice, Inbred A,
pubmed-meshheading:2496163-Mice, Inbred BALB C,
pubmed-meshheading:2496163-Mice, Inbred C3H,
pubmed-meshheading:2496163-Mice, Inbred C57BL,
pubmed-meshheading:2496163-Mice, Inbred DBA,
pubmed-meshheading:2496163-Species Specificity,
pubmed-meshheading:2496163-Spleen,
pubmed-meshheading:2496163-T-Lymphocytes,
pubmed-meshheading:2496163-Toxoplasmosis, Animal
|
| pubmed:year |
1989
|
| pubmed:articleTitle |
Immune responses associated with early survival after peroral infection with Toxoplasma gondii.
|
| pubmed:affiliation |
Department of Medicine, Michael Reese Medical Center, Chicago, IL 60616.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|