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The role of gamma interferon in acquired host resistance against Staphylococcus aureus infection in mice
Author(s) -
Sasaki Sanae,
Tagawa YohIchi,
Iwakura Yoichiro,
Nakane Akio
Publication year - 2006
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.2005.00037.x
Subject(s) - staphylococcus aureus , interferon gamma , biology , spleen , antibody , monoclonal antibody , microbiology and biotechnology , staphylococcal infections , virology , immunology , immune system , bacteria , genetics
We investigated the expression of an acquired host resistance against Staphylococcus aureus infection in mice. When C57BL/6 mice were immunized with viable S. aureus and challenged with S. aureus eight weeks later, the elimination of S. aureus from the spleen and liver was enhanced in the immunized mice compared with the nonimmunized mice. When gamma interferon (IFN‐γ −/− ) mice were immunized and challenged, the bacterial numbers in the organs of immunized mice were comparable to those in the nonimmunized mice, suggesting that IFN‐γ plays a critical role in an acquired host resistance against S. aureus infection. IFN‐γ −/− mice produced the lower level of anti‐ S. aureus immunoglobulin M (IgM) and IgG2a antibodies compared with C57BL/6 mice. To elucidate the role of IFN‐γ produced during a challenge with S. aureus , a single injection of anti‐IFN‐γ monoclonal antibody to mice was carried out 1 h before challenge. An acquired resistance against S. aureus infection was inhibited by injecting with anti‐IFN‐γ monoclonal antibody. However, anti‐IFN‐γ monoclonal antibody treatment failed to modulate anti‐ S. aureus IgM, IgG1 or IgG2a responses in these animals. These results demonstrated that IFN‐γ is required for an acquired resistance against S. aureus infection in mice. However, IFN‐γ induced during the challenge failed to affect the secondary antibody responses.

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