Exacerbation of invasive candida albicans infection by commensal bacteria or a glycolipid through IFN- Produced in part by iNKT cells

Norihito Tarumoto, Yuki Kinjo, Naoki Kitano, Daisuke Sasai, Keigo Ueno, Akiko Okawara, Yuina Izawa, Minoru Shinozaki, Hiroshi Watarai, Masaru Taniguchi, Haruko Takeyama, Shigefumi Maesaki, Kazutoshi Shibuya, Yoshitsugu Miyazaki

研究成果: Article査読

10 被引用数 (Scopus)

抄録

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-KO) mice. In the C. albicans-infected, glycolipid-treated mice, the number of neutrophils in the blood and bone marrow dramatically decreased in an IFN--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- and iNKT cells.Conclusions. Our results indicate that coinfecting commensal bacteria exacerbate C. albicans infection through IFN- produced, in part, by iNKT cells.

本文言語English
ページ(範囲)799-810
ページ数12
ジャーナルJournal of Infectious Diseases
209
5
DOI
出版ステータスPublished - 2014 3

ASJC Scopus subject areas

  • Immunology and Allergy
  • Infectious Diseases

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