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猪带绦虫有利于孢子丝菌感染引起的迁延性皮肤损伤:Dectin-1 和 IL-17 对于清除这种真菌是可有可无的。

Taenia taeniaeformis in rat favors protracted skin lesions caused by Sporothrix schenckii infection: Dectin-1 and IL-17 are dispensable for clearance of this fungus.

机构信息

Department of Dermatology and Venereology, Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong Province, China.

出版信息

PLoS One. 2012;7(12):e52514. doi: 10.1371/journal.pone.0052514. Epub 2012 Dec 20.

Abstract

We occasionally found that cestode Taenia taeniaeformis in rats favored Sporothrix schenckii infection and survival, causing protracted cutaneous lesions. In this study, we compared the pathology and cytokines profile of rats co-infected with the two pathogens and infected with S. schenckii alone to explore underlying mechanisms. In the co-infection group, there was high expression of β-glucan receptor Dectin-1 in the cutaneous lesions and no multinucleated giant cells, but in the S. schenckii infection group the opposite was observed. Cytokines profiles demonstrated an expected finding that IL-4, commonly expressed in helminth and fungus infection, is undetectable in the two infection groups. In the single fungal infection group, cytokines IFN-γ, IL-10 and IL-17 kept increasing in the first few weeks of infection to a peak which was followed by gradual decrease. This study showed that Dectin-1 and IL-17, which were believed to be the major anti-fungus mechanisms, are Th2 independent and dispensable for clearance of S. schenckii infection, suggesting that S. schenckii has a different molecular recognition pattern and evokes anti-infection mechanisms other than Dectin-1 and IL-17.

摘要

我们偶尔发现,大鼠体内的带绦虫囊尾蚴有利于申克孢子丝菌感染和存活,导致皮肤病变迁延不愈。在这项研究中,我们比较了两种病原体共同感染和单独感染申克孢子丝菌的大鼠的病理学和细胞因子谱,以探讨潜在的机制。在共同感染组中,皮肤病变中β-葡聚糖受体 Dectin-1 表达较高,没有多核巨细胞,但在单独感染申克孢子丝菌组中则相反。细胞因子谱显示了一个预期的发现,即通常在寄生虫和真菌感染中表达的 IL-4 在两个感染组中均无法检测到。在单独真菌感染组中,IFN-γ、IL-10 和 IL-17 等细胞因子在感染的前几周逐渐增加到峰值,随后逐渐减少。本研究表明,被认为是主要抗真菌机制的 Dectin-1 和 IL-17 不依赖于 Th2,对于清除申克孢子丝菌感染是可有可无的,这表明申克孢子丝菌具有不同的分子识别模式,并引发了不同于 Dectin-1 和 IL-17 的抗感染机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7eae/3527553/413a48d8fb64/pone.0052514.g001.jpg

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