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. 2000 Sep;68(9):5126-31.
doi: 10.1128/IAI.68.9.5126-5131.2000.

V体育官网 - Interleukin 18 restores defective Th1 immunity to Candida albicans in caspase 1-deficient mice

A Mencacci  1 , A Bacci, E Cenci, C Montagnoli, S Fiorucci, A Casagrande, R A Flavell, F Bistoni, L Romani
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Interleukin 18 restores defective Th1 immunity to Candida albicans in caspase 1-deficient mice (V体育2025版)

A Mencacci et al. Infect Immun. 2000 Sep.

"V体育平台登录" Abstract

Caspase 1, formerly designated interleukin 1beta (IL-1beta)-converting enzyme, processes pro-IL-1beta and pro-IL-18 to yield active cytokines that play a pivotal role in inflammation and cell activation. We show here the effect of caspase 1 deficiency on the inflammatory and adaptive immune responses to the fungus Candida albicans VSports手机版. Caspase 1 deficiency did not affect susceptibility to primary systemic infection with the fungus, as revealed by survival and fungal growth. However, Th1-mediated resistance to reinfection was greatly impaired in caspase 1-deficient mice, and this correlated with low-level production of IL-12 and gamma interferon. Early in infection, production of these cytokines and that of tumor necrosis factor alpha, IL-6, and, interestingly, IL-1beta occurred normally in caspase 1-deficient mice, while that of IL-18 was severely impaired. Exogenous administration of IL-18, more than IL-12, restored the Th1-mediated resistance to the infection. We conclude that, while caspase 1 is not indispensable for release of mature IL-1beta in candidiasis, the caspase 1-dependent production of IL-18 may represent an important and novel pathway for the expression of sustained Th1 reactivity to the fungus. .

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Figures

FIG. 1
FIG. 1
Antifungal effector functions of macrophages and neutrophils from caspase 1−/− (solid bars) and caspase 1+/+ C57BL/6 (open bars) mice, uninfected or upon primary i.v. infection with C. albicans. Three days after infection, splenic adherent macrophages and elicited peritoneal neutrophils were assessed for their ability to kill yeast cells and to secrete NO in vitro. Assays were done as described in Materials and Methods. ∗, P < 0.05, caspase 1−/− versus caspase 1+/+ mice.
FIG. 2
FIG. 2
Cytokine and cytokine receptor gene expression in caspase 1−/− and caspase 1+/+ C57BL/6 mice upon C. albicans infection. Mice were either uninfected (lanes 1) or reinfected (lanes 2) with virulent CA-6, 14 days after the primary infection with PCA-2. Levels of IFN-γ, IL-4, IL-12Rβ2, and IL-18R mRNA (in CD4+ T splenocytes) and of IL-12p40 (in splenic macrophages) were determined by RT-PCR, 3 days after reinfection. C, HPRT- or cytokine- or cytokine receptor-specific control. N, no DNA added to the amplification mix during PCR. Mφ, macrophages.
FIG. 3
FIG. 3
Production of proinflammatory cytokines in caspase 1−/− (solid bars) and caspase 1+/+ (open bars) mice uninfected or infected with C. albicans. Mice were i.v. infected with 106 PCA-2 cells and assessed 3 days later for cytokine production in culture supernatants of antigen-stimulated splenocytes. Levels of cytokines were determined by means of cytokine-specific ELISA. Cytokine levels in culture supernatants of unstimulated responder cells were below the detection limit of the assay, indicated by < in the y axis. ∗, P < 0.05, caspase 1−/− versus caspase 1+/+ mice.
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