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Interleukin-12 promotes a chronic intestinal nematode infection
A J Bancroft1, K J Else, J P Sypek
1School of Biological Sciences, University of Manchester, GB.
European Journal of Immunology
|April 1, 1997
Summary
Interleukin-12 (IL-12) drives a strong T helper 1 (Th1) response, promoting chronic Trichuris muris infection in mice. This effect is dependent on interferon-gamma (IFN-gamma) and can be induced even after infection begins.
Area of Science:
- Immunology
- Parasitology
- Infectious Disease
Background:
- Immune responses, specifically T helper 1 (Th1) and T helper 2 (Th2) pathways, dictate resistance or susceptibility to the intestinal parasite Trichuris muris.
- The cytokine environment during antigen presentation is critical for immune response polarization, but the exact factors remain unclear.
- Interleukin-12 (IL-12) is a key cytokine linking innate and adaptive immunity, promoting Th1 responses and interferon-gamma (IFN-gamma) production.
Purpose of the Study:
- To investigate the role of IL-12 in modulating the immune response to Trichuris muris infection.
- To determine if IL-12 administration can alter the course of T. muris infection in normally resistant mice.
- To elucidate the mechanisms underlying IL-12's effects on T. muris infection, particularly the involvement of IFN-gamma.
Main Methods:
- Administration of IL-12 to BALB/K mice infected with Trichuris muris.
- Monitoring of parasite-specific antibody levels, including IgG2a (a Th1 marker).
- Assessment of IL-12's effects in the presence of an anti-IFN-gamma monoclonal antibody (mAb).
Main Results:
- IL-12 treatment promoted chronic T. muris infection in resistant mice by inducing a strong Th1 response.
- Parasite-specific IgG2a levels were significantly upregulated, while some Th2 parameters were downregulated.
- The Th1-inducing and infection-prolonging effects of IL-12 were dependent on IFN-gamma, as demonstrated by abrogation with anti-IFN-gamma mAb.
- IL-12 administration up to one week post-infection remained effective in promoting a Th1 response.
Conclusions:
- IL-12, by driving a Th1 response, can convert a normally self-limiting T. muris infection into a chronic one.
- IFN-gamma is essential for IL-12-mediated exacerbation of T. muris infection.
- These findings highlight the complex role of IL-12 in parasitic infections and suggest therapeutic strategies targeting cytokine balance.