Exacerbation of Invasive Candida Albicans Infection by Commensal Bacteria or a Glycolipid Through IFN-γ Produced in Part by INKT Cells

Overview

Journal J Infect Dis

Publisher Oxford University Press

Specialty Infectious Diseases

Date 2013 Oct 8

PMID 24096333

Citations 11

Authors

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

Affiliations

Soon will be listed here.

Abstract

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.

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