Immune responses associated with early survival after peroral infection with Toxoplasma gondii

R. McLeod, P. Eisenhauer, D. Mack, C. Brown, G. Filice, G. Spitalny

Research output: Contribution to journalArticlepeer-review

86 Scopus citations

Abstract

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 < 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 < 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 < 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 < 0.05) and produced significantly more IFN-γ in culture with (p = 0.009) or without (p < 0.05) Toxoplasma Ag than spleen cells from infected resistant mice. Infection increased serum levels of IFN-γ 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.

Original languageEnglish (US)
Pages (from-to)3247-3255
Number of pages9
JournalJournal of Immunology
Volume142
Issue number9
StatePublished - 1989

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