Interferon-γ limits toxoplasma gondii proliferation in gut and dissemination after peroral infection

G. A. Filice, D. Delong, P. E. Riciputi, C. R. Clabots

Research output: Contribution to journalArticlepeer-review

Abstract

OBJECTIVE: Immunization to prevent congenital or reactivation toxoplasmosis would be desirable. For immunization to be effective, we propose that it would have to prevent parasitemia after ingestion. This study was done to determine if Interferon (IFN)γ limits T. gondii proliferation in gut or limits dissemination after peroral infection. METHODS: C57BL/6 IFNγ knockout (-/-) and control (+/+) mice were infected perorally with 300 Me49 T. gondii tissue cysts. Time to severe illness was documented and mice were euthanatized. At regular intervals, T. gondii tachyzoites were detected in tissues by immunohistology and the T. gondii B1 gene was detected by PCR. RESULTS: All IFNγ -/- mice were severely ill by 9 days and had to be euthanatized. 60% of IFNγ +/+ mice became this ill by this time, but 40% survived. By immunohistology, tachyzoites multiplied to greater densities in Peyer's patches of IFNγ -/- mice than in +/+ mice. By both immunohistology and B1 gene detection, T. gondii appeared earlier and multiplied to a greater extent in mesenteric lymph nodes of IFNγ -/- mice. Similarly, T. gondii disseminated earlier and to a greater extent in liver and spleen in IFNγ -/- mice. CONCLUSIONS: The results suggest that IFNγ limits T. gondii replication in gut and mesenteric lymph node. IFNγ prevents T. gondii dissemination either by limiting its escape from the gut or by limiting replication in distant organs. Effective immunization may need to enable gut immune cells to produce IFNγ quickly in response to challenge infection.

Original languageEnglish (US)
Number of pages1
JournalClinical Infectious Diseases
Volume25
Issue number2
StatePublished - 1997

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