| Autor: |
McDonald, S.A.C., Bejaj-Elliott, M., Smith, P.T., Ballinger, A.B., McDonald, V. |
| Předmět: |
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| Zdroj: |
Gut; Apr2003 Supplement 1, Vol. 52, pA55, 2p |
| Abstrakt: |
Introduction: Immunological control of Cryptosporidium parvum infection is dependent on a Th1 response with interferon-γ production. However, in a neonatal murine infection model we have shown that the Th2 cytokine IL-4 is also involved as BALB/c lL-4 knockout (KO) mice develop more intense oocyst shedding at the peak of infection (Day 7) than wild-type mice. Paradoxically, at this time, no increase in lb4 mRNA could be detected in the intestines of wild-type mice. The aim of this study was to characterise further IL-4 involvement in the early priming of immunity to C parvum. Methods: Neonatal BALB/c wild-type or SCID mice (which lack T and B cells) were infected at 4 or 7 days of age with a cervine isolate of C parvum and infections were subsequently measured microscopically from acid-fast stained smears of colonic contents. Murine recombinant IL-4 (1.0 and 0.75µg) was injected sc prior to infection and 6 h later. Rat anti-IL-4 IgG monoclonal antibody 11B11 (100µg) was injected prior to infection or 4 days post-infection. Results: Injection of BALB/c mice with IL-4 decreased the level of C parvum reproduction on day 7 by a factor of 4.6. Administration of anti-IL-4 to BALB/c mice prior to infection-but not 4 days post-infection—increased susceptibility to infection. To determine if an lL-4 dependent innate mechanism was at work, SCID mice were given anti-IL-4 prior to infection, but this did not increase parasite reproduction. Conclusion: IL-4 may act early in infection to boost the adaptive immune response to the intracellular mucosal parasite, C parvum. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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