Modification of Subclinical Toxoplasmosis in Mice by Cortisone, 6-Mercaptopurine and Splenectomy *

Stahl, William L.; Matsubayashi, Hisakichi; Akao, Shinkichi

doi:10.4269/ajtmh.1966.15.869

Cited by 31 publications

(12 citation statements)

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“…Multiple studies have addressed the contribution of the spleen to the response to T. gondii, and the outcomes have varied by study: certain groups have found improved survival in splenectomized mice with lower parasite burdens and faster immune responses (24), while others demonstrate increased susceptibility to infection (44). In current studies, although splenectomized mice challenged with T. gondii demonstrated an initial defect in antibody production, they exhibited levels of parasite-specific antibody similar to those of WT mice by the later stages of infection, as well as comparable T and B cell responses in the LN.…”

Section: Discussionmentioning

confidence: 99%

Infection with Toxoplasma gondii Alters Lymphotoxin Expression Associated with Changes in Splenic Architecture

et al. 2012

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c B cell responses are required for resistance to Toxoplasma gondii; however, the events that lead to production of class-switched antibodies during T. gondii infection have not been defined. Indeed, mice challenged with the parasite exhibited an expansion of T follicular helper cells and germinal center B cells in the spleen. Unexpectedly, this was not associated with germinal center formation and was instead accompanied by profound changes in splenic organization. This phenomenon was transient and was correlated with a decrease in expression of effector proteins that contribute to splenic organization, including lymphotoxins ␣ and ␤. The importance of lymphotoxin was confirmed, as the use of a lymphotoxin ␤ receptor agonist results in partial restoration of splenic structure. Splenectomized mice were used to test the splenic contribution to the antibody response during T. gondii infection. Analysis of splenectomized mice revealed delayed kinetics in the production of parasite-specific antibody, but the mice did eventually develop normal levels of parasite-specific antibody. Together, these studies provide a better understanding of how infection with T. gondii impacts the customized structures required for the optimal humoral responses to the parasite and the role of lymphotoxin in these events. The intracellular protozoan parasite Toxoplasma gondii is the causative agent of toxoplasmosis, an important opportunistic infection of humans and livestock (20,38). In mice, the acute stage of infection with T. gondii is characterized by systemic parasite dissemination and significant T and B cell activation. Control of parasite replication and transition to the chronic phase of infection are dependent on T and B cells. Although this infection has been used as a model to study cell-mediated immunity, antibodies are also critical for resistance to T. gondii; B cell-deficient mice succumb to T. gondii during the chronic phase of infection but can be rescued by passive antibody transfer (25,39). Despite these initial studies, many questions remain about the T and B cell interactions that promote antibody responses during infection.It has long been established that antigen-specific antibody responses develop within germinal centers (GCs), specialized regions within the lymphoid follicle that promote the T cell-B cell interactions that are crucial for isotype switching and affinity maturation. Recent work has demonstrated that the T cells involved in these events are T follicular helper (TFH) cells, a T helper cell subset defined by expression of the transcription factor Bcl6 and the chemokine receptor CXCR5, which promotes entry into the GC (5, 23, 34, 41, 51; for a review, see references 9 and 27.) This has led to the idea that the TFH cell subset is defined, at least in part, by location; although TFH cells have been found both within and outside the GC, it is unclear whether TFH cells outside GCs retain their antibody-promoting function (52).The organization of secondary lymphoid organs is configured to facilitate the v...

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Section: Discussionmentioning

confidence: 99%

Infection with Toxoplasma gondii Alters Lymphotoxin Expression Associated with Changes in Splenic Architecture

et al. 2012

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“…Use of corticosteroids in experimentally infected laboratory animals resulted in death of most of the acutely and chronically infected who developed reactivation of infection [390][391][392][393][394][395]. Pathological examination of these animals demonstrated fatal encephalitis or pneumonia, which was associated with a characteristically absent inflammatory response [394,396].…”

Section: Role Of Corticosteroid Administrationmentioning

confidence: 99%

Immunopathogenesis of toxoplasmosis

Hegab

Al-Mutawa²

2003

Clinical and Experimental Medicine

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Toxoplasmosis is a ubiquitous infection affecting 500 million persons around the world, with a range of incidence 12%-90%, increasing with age, education, crowding and sanitary habits. Cats are the definitive host. Infection is primarily congenital but acquired ocular infection has been documented. The review focuses on the immunopathogenesis of toxoplasmosis with emphasis on the eye problem due to its morbidity. The response to infection correlates with both parasitic and retinal antigens. The clinical picture and histopathology is a reflection of the immune response which constitutes early humeral response which presents both systemically and locally primary infection and is elevated with reactivation. This is followed by the cellular response, varying from low grade monocular infilterate a total tissue destruction with response of live parasites especially in immuno-compromised patients. Penetration of the parasite and its enclosure within the parasitophorous vacuole and its eneyst all make its eradicatier impossible. This reflects the variability of antiparasitic therapy that include folate antagonists, macrolides, hydroxy naphthoquindones and fluoroquinolones. Use of corticosteroid should be limited to severe reactions and should be associated with specific therapy.

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“…A lethal effect of corticosteroids in acute toxoplasmosis was found in the majority of animal studies (mice and rabbits)20-24; however, the therapy also induced less effective resistance to subsequent reactivations 22. In contrast with untreated animals, in corticosteroid treated mice with acute toxoplasmosis, persistence of free parasites together with cysts in the brain and lung tissue was observed 20…”

Section: Effect Of Corticosteroids On Toxoplasmosis: Animal Studiesmentioning

confidence: 99%

“…In contrast with untreated animals, in corticosteroid treated mice with acute toxoplasmosis, persistence of free parasites together with cysts in the brain and lung tissue was observed 2021Furthermore, cyst formation in the brain started earlier and was more prolific in corticosteroid treated mice 22. However, corticosteroid treated rabbits with ocular toxoplasmosis had localised retinal lesions with preservation of normal tissue in contrast with non-treated animals in which retinal destruction was considerably more massive and areas of normal retina were not encountered 23…”

Section: Effect Of Corticosteroids On Toxoplasmosis: Animal Studiesmentioning

confidence: 99%

Sense and nonsense of corticosteroid administration in the treatment of ocular toxoplasmosis

Bosch-Driessen

Rothová

1998

British Journal of Ophthalmology

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Modification of Subclinical Toxoplasmosis in Mice by Cortisone, 6-Mercaptopurine and Splenectomy *

Cited by 31 publications

References 0 publications

Infection with Toxoplasma gondii Alters Lymphotoxin Expression Associated with Changes in Splenic Architecture

Infection with Toxoplasma gondii Alters Lymphotoxin Expression Associated with Changes in Splenic Architecture

Immunopathogenesis of toxoplasmosis

Sense and nonsense of corticosteroid administration in the treatment of ocular toxoplasmosis

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