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烟曲霉与肺上皮细胞的相互作用。

Interaction of the pathogenic mold Aspergillus fumigatus with lung epithelial cells.

机构信息

Department of Clinical Microbiology and Immunology, Aspergillus and Antifungal Research Laboratory, Sackler School of Medicine, Tel-Aviv University Ramat-Aviv, Tel-Aviv, Israel.

出版信息

Front Microbiol. 2012 Sep 26;3:346. doi: 10.3389/fmicb.2012.00346. eCollection 2012.

DOI:10.3389/fmicb.2012.00346
PMID:23055997
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3458433/
Abstract

Aspergillus fumigatus is an opportunistic environmental mold that can cause severe allergic responses in atopic individuals and poses a life-threatening risk for severely immunocompromised patients. Infection is caused by inhalation of fungal spores (conidia) into the lungs. The initial point of contact between the fungus and the host is a monolayer of lung epithelial cells. Understanding how these cells react to fungal contact is crucial to elucidating the pathobiology of Aspergillus-related disease states. The experimental systems, both in vitro and in vivo, used to study these interactions, are described. Distinction is made between bronchial and alveolar epithelial cells. The experimental findings suggest that lung epithelial cells are more than just "innocent bystanders" or a purely physical barrier against infection. They can be better described as an active extension of our innate immune system, operating as a surveillance mechanism that can specifically identify fungal spores and activate an offensive response to block infection. This response includes the internalization of adherent conidia and the release of cytokines, antimicrobial peptides, and reactive oxygen species. In the case of allergy, lung epithelial cells can dampen an over-reactive immune response by releasing anti-inflammatory compounds such as kinurenine. This review summarizes our current knowledge regarding the interaction of A. fumigatus with lung epithelial cells. A better understanding of the interactions between A. fumigatus and lung epithelial cells has therapeutic implications, as stimulation or inhibition of the epithelial response may alter disease outcome.

摘要

烟曲霉是一种机会性环境霉菌,可导致特应性个体发生严重过敏反应,并对严重免疫功能低下的患者构成生命威胁。感染是由真菌孢子(分生孢子)吸入肺部引起的。真菌与宿主最初接触的部位是一层肺上皮细胞。了解这些细胞如何对真菌接触做出反应对于阐明与曲霉相关疾病状态的病理生物学至关重要。本文描述了用于研究这些相互作用的体外和体内实验系统。区分了支气管和肺泡上皮细胞。实验结果表明,肺上皮细胞不仅仅是“无辜的旁观者”或感染的纯物理屏障。它们可以更好地描述为我们固有免疫系统的积极延伸,作为一种监视机制,可以特异性识别真菌孢子并激活阻止感染的进攻性反应。这种反应包括对附着分生孢子的内化以及细胞因子、抗菌肽和活性氧物质的释放。在过敏的情况下,肺上皮细胞可以通过释放抗炎化合物(如犬尿氨酸)来抑制过度的免疫反应。这篇综述总结了我们目前对烟曲霉与肺上皮细胞相互作用的认识。更好地了解烟曲霉与肺上皮细胞之间的相互作用具有治疗意义,因为刺激或抑制上皮反应可能会改变疾病的结果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f326/3458433/fe03b769860a/fmicb-03-00346-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f326/3458433/ed6f93cee653/fmicb-03-00346-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f326/3458433/04a7d35d0384/fmicb-03-00346-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f326/3458433/8bdde3da668a/fmicb-03-00346-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f326/3458433/fe03b769860a/fmicb-03-00346-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f326/3458433/ed6f93cee653/fmicb-03-00346-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f326/3458433/04a7d35d0384/fmicb-03-00346-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f326/3458433/8bdde3da668a/fmicb-03-00346-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f326/3458433/fe03b769860a/fmicb-03-00346-g0004.jpg

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