The Journal of Immunology, Vol 142, Issue 9 3247-3255, Copyright © 1989 by American Association of Immunologists

ARTICLES

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

R McLeod, P Eisenhauer, D Mack, C Brown, G Filice and G Spitalny
Department of Medicine, Michael Reese Medical Center, Chicago, IL 60616.

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.

This article has been cited by other articles:

				F. Lu, S. Huang, M. S. Hu, and L. H. Kasper Experimental Ocular Toxoplasmosis in Genetically Susceptible and Resistant Mice Infect. Immun., August 1, 2005; 73(8): 5160 - 5165. [Abstract] [Full Text] [PDF]

				N. Rachinel, D. Buzoni-Gatel, C. Dutta, F. J. D. Mennechet, S. Luangsay, L. A. Minns, M. E. Grigg, S. Tomavo, J. C. Boothroyd, and L. H. Kasper The Induction of Acute Ileitis by a Single Microbial Antigen of Toxoplasma gondii J. Immunol., August 15, 2004; 173(4): 2725 - 2735. [Abstract] [Full Text] [PDF]

				V. Martin, A. Supanitsky, P. C. Echeverria, S. Litwin, T. Tanos, A. R. De Roodt, E. A. Guarnera, and S. O. Angel Recombinant GRA4 or ROP2 Protein Combined with Alum or the gra4 Gene Provides Partial Protection in Chronic Murine Models of Toxoplasmosis Clin. Vaccine Immunol., July 1, 2004; 11(4): 704 - 710. [Abstract] [Full Text]

				D. G. Mordue and L. D. Sibley A novel population of Gr-1+-activated macrophages induced during acute toxoplasmosis J. Leukoc. Biol., December 1, 2003; 74(6): 1015 - 1025. [Abstract] [Full Text]

				B. Fux, C. V. Rodrigues, R. W. Portela, N. M. Silva, C. Su, D. Sibley, R. W. A. Vitor, and R. T. Gazzinelli Role of Cytokines and Major Histocompatibility Complex Restriction in Mouse Resistance to Infection with a Natural Recombinant Strain (Type I-III) of Toxoplasma gondii Infect. Immun., November 1, 2003; 71(11): 6392 - 6401. [Abstract] [Full Text] [PDF]

				C. M. Tato, A. Villarino, J. H. Caamano, M. Boothby, and C. A. Hunter Inhibition of NF-{kappa}B Activity in T and NK Cells Results in Defective Effector Cell Expansion and Production of IFN-{gamma} Required for Resistance to Toxoplasma gondii J. Immunol., March 15, 2003; 170(6): 3139 - 3146. [Abstract] [Full Text] [PDF]

				J. J. Johnson, C. W. Roberts, C. Pope, F. Roberts, M. J. Kirisits, R. Estes, E. Mui, T. Krieger, C. R. Brown, J. Forman, et al. In Vitro Correlates of Ld-Restricted Resistance to Toxoplasmic Encephalitis and Their Critical Dependence on Parasite Strain J. Immunol., July 15, 2002; 169(2): 966 - 973. [Abstract] [Full Text] [PDF]

				Y. Suzuki, A. Sher, G. Yap, D. Park, L. E. Neyer, O. Liesenfeld, M. Fort, H. Kang, and E. Gufwoli IL-10 Is Required for Prevention of Necrosis in the Small Intestine and Mortality in Both Genetically Resistant BALB/c and Susceptible C57BL/6 Mice Following Peroral Infection with Toxoplasma gondii J. Immunol., May 15, 2000; 164(10): 5375 - 5382. [Abstract] [Full Text] [PDF]

				M. Vercammen, T. Scorza, K. Huygen, J. De Braekeleer, R. Diet, D. Jacobs, E. Saman, and H. Verschueren DNA Vaccination with Genes Encoding Toxoplasma gondii Antigens GRA1, GRA7, and ROP2 Induces Partially Protective Immunity against Lethal Challenge in Mice Infect. Immun., January 1, 2000; 68(1): 38 - 45. [Abstract] [Full Text] [PDF]

				I. A. Khan and M. Moretto Role of Gamma Interferon in Cellular Immune Response against Murine Encephalitozoon cuniculi Infection Infect. Immun., April 1, 1999; 67(4): 1887 - 1893. [Abstract] [Full Text] [PDF]

				I. A. Khan, J. D. Schwartzman, T. Matsuura, and L. H. Kasper A dichotomous role for nitric oxide during acute Toxoplasma gondii infection in mice PNAS, December 9, 1997; 94(25): 13955 - 13960. [Abstract] [Full Text] [PDF]