| Autor: |
Tarumoto, Norihito, Kinjo, Yuki, Kitano, Naoki, Sasai, Daisuke, Ueno, Keigo, Okawara, Akiko, Izawa, Yuina, Shinozaki, Minoru, Watarai, Hiroshi, Taniguchi, Masaru, Takeyama, Haruko, Maesaki, Shigefumi, Shibuya, Kazutoshi, Miyazaki, Yoshitsugu |
| Zdroj: |
Journal of Infectious Diseases; Mar2014, Vol. 209 Issue 5, p799-810, 12p |
| Abstrakt: |
Background: The commensal yeast Candida albicans is a major cause of invasive fungal infections. Despite treatment with antifungal agents, the mortality rate attributed to these types of infection is high. Although numerous cases have been reported regarding a poor outcome for patients with bacterial and C. albicans coinfection, the mechanisms by which the coinfecting bacteria exacerbate the C. albicans infection remain elusive.Methods and Results: We evaluated how glycolipid-mediated activation of invariant natural killer T (iNKT) cells affects the clearance of C. albicans. Surprisingly, C. albicans-infected, glycolipid-treated mice exhibited significantly lower survival rates, increased fungal burden, and higher interleukin (IL)-6 production in the kidneys compared with control mice. Glycolipid-induced exacerbation of C. albicans infection was not observed in interferon-gamma knockout (IFN-γKO) mice. In the C. albicans-infected, glycolipid-treated mice, the number of neutrophils in the blood and bone marrow dramatically decreased in an IFN-γ-dependent manner. Furthermore, mice that were coinfected with C. albicans and nonfermentative gram-negative commensal bacteria exhibited increased fungal burden and inflammatory cytokine production in the kidneys that were dependent on IFN-γ and iNKT cells.Conclusions: Our results indicate that coinfecting commensal bacteria exacerbate C. albicans infection through IFN-γ produced, in part, by iNKT cells. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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