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Interleukin-6-deficient mice are highly susceptible to Giardia lamblia infection but exhibit normal intestinal immunoglobulin A responses against the parasite.

Abstract
In the present study, interleukin-6 (IL-6)-deficient mice were infected with Giardia lamblia clone GS/M-83-H7. Murine IL-6 deficiency did not affect the synthesis of parasite-specific intestinal immunoglobulin A. However, in contrast to wild-type mice, IL-6-deficient animals were not able to control the acute phase of parasite infection. Reverse transcription-PCR-based quantitation of cytokine mRNA levels in peripheral lymph node cells exhibited a short-term up-regulation of IL-4 expression in IL-6-deficient mice that seemed to be associated with failure in controlling the parasite population. This observation suggests a further elucidation of IL-4-dependent, Th2-type regulatory processes regarding their potential to influence the course of G. lamblia infection in the experimental murine host.
AuthorsMarianne Bienz, Wen Juan Dai, Monika Welle, Bruno Gottstein, Norbert Müller
JournalInfection and immunity (Infect Immun) Vol. 71 Issue 3 Pg. 1569-73 (Mar 2003) ISSN: 0019-9567 [Print] United States
PMID12595479 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Antibodies, Protozoan
  • Immunoglobulin A
  • Interleukin-6
  • Interleukin-4
  • Interferon-gamma
Topics
  • Animals
  • Antibodies, Protozoan (biosynthesis)
  • Disease Susceptibility
  • Enzyme-Linked Immunosorbent Assay
  • Female
  • Giardia lamblia (immunology)
  • Giardiasis (immunology)
  • Immunoglobulin A (biosynthesis)
  • Interferon-gamma (biosynthesis)
  • Interleukin-4 (biosynthesis)
  • Interleukin-6 (deficiency, physiology)
  • Mice
  • Mice, Inbred C57BL
  • Reverse Transcriptase Polymerase Chain Reaction

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