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侵袭性肺曲霉病白细胞介素-6缺陷小鼠的抗真菌效应活性受损,但炎症细胞募集未受影响。

Impaired antifungal effector activity but not inflammatory cell recruitment in interleukin-6-deficient mice with invasive pulmonary aspergillosis.

作者信息

Cenci E, Mencacci A, Casagrande A, Mosci P, Bistoni F, Romani L

机构信息

Microbiology Section, Department of Experimental Medicine and Biochemical Sciences, University of Perugia, 06122 Perugia, Italy.

出版信息

J Infect Dis. 2001 Sep 1;184(5):610-7. doi: 10.1086/322793. Epub 2001 Jul 30.

DOI:10.1086/322793
PMID:11494166
Abstract

A murine model of infection, in which immunocompetent or immunosuppressed interleukin-6-deficient (IL-6(-/-)) mice were infected intranasally with Aspergillus fumigatus conidia and were monitored for parameters of fungal colonization and innate and adaptive immunity, was used to assess the role of IL-6 in invasive pulmonary aspergillosis (IPA). The results indicate that IL-6(-/-) mice were more susceptible than wild-type mice to IPA. Susceptibility was associated with increased inflammatory pathology, decreased antifungal effector functions of phagocytes, and impaired development of protective type 1 responses. Exposure to exogenous IL-6 restored antifungal effector activity.

摘要

一种感染小鼠模型被用于评估白细胞介素-6(IL-6)在侵袭性肺曲霉病(IPA)中的作用,在该模型中,免疫功能正常或免疫抑制的IL-6缺陷(IL-6(-/-))小鼠经鼻内接种烟曲霉菌分生孢子,并监测真菌定植参数以及固有免疫和适应性免疫。结果表明,IL-6(-/-)小鼠比野生型小鼠对IPA更易感。易感性与炎症病理增加、吞噬细胞抗真菌效应功能降低以及保护性1型反应的发育受损有关。暴露于外源性IL-6可恢复抗真菌效应活性。

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