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全身性念珠菌病伴发低胰岛素血症-高血糖症小鼠吞噬性腹腔细胞的迁移。

Trafficking of phagocytic peritoneal cells in hypoinsulinemic-hyperglycemic mice with systemic candidiasis.

机构信息

Departamento de Ciências Biológicas, Laboratório de Imunopatologia Experimental (LIPE), UNESP - Univ Estadual Paulista, Bauru, SP 17033-360, Brazil.

出版信息

BMC Infect Dis. 2013 Mar 25;13:147. doi: 10.1186/1471-2334-13-147.

Abstract

BACKGROUND

Candidemia is a severe fungal infection that primarily affects hospitalized and/or immunocompromised patients. Mononuclear phagocytes have been recognized as pivotal immune cells which act in the recognition of pathogens, phagocytosis, inflammation, polarization of adaptive immune response and tissue repair. Experimental studies have showed that the systemic candidiasis could be controlled by activated peritoneal macrophages. However, the mechanism to explain how these cells act in distant tissue during a systemic fungal infection is still to be elucidated. In the present study we investigate the in vivo trafficking of phagocytic peritoneal cells into infected organs in hypoinsulinemic-hyperglycemic (HH) mice with systemic candidiasis.

METHODS

The red fluorescent vital dye PKH-26 PCL was injected into the peritoneal cavity of Swiss mice 24 hours before the intravenous inoculation with Candida albicans. After 24 and 48 hours and 7 days of infection, samples of the spleen, liver, kidneys, brain and lungs were submitted to the microbiological evaluation as well as to phagocytic peritoneal cell trafficking analyses by fluorescence microscopy.

RESULTS

In the present study, PKH+ cells were observed in the peritoneum, kidney, spleen and liver samples from all groups. In infected mice, we also found PKH+ cells in the lung and brain. The HH condition did not affect this process.

CONCLUSIONS

In the present study we have observed that peritoneal phagocytes migrate to tissues infected by C. albicans and the HH condition did not interfere in this process.

摘要

背景

念珠菌血症是一种严重的真菌感染,主要影响住院和/或免疫功能低下的患者。单核吞噬细胞已被认为是关键的免疫细胞,它们在识别病原体、吞噬作用、炎症、适应性免疫反应的极化和组织修复中发挥作用。实验研究表明,系统性念珠菌病可以通过激活的腹膜巨噬细胞来控制。然而,解释这些细胞在系统性真菌感染时如何在远处组织中发挥作用的机制仍有待阐明。在本研究中,我们研究了胰岛素缺乏-高血糖(HH)小鼠系统性念珠菌病中吞噬性腹膜细胞向感染器官的体内迁移。

方法

在静脉接种白色念珠菌前 24 小时,将红色荧光活染料 PKH-26 PCL 注入瑞士小鼠的腹腔。在感染后 24 小时、48 小时和 7 天,对脾、肝、肾、脑和肺的样本进行微生物学评估,并通过荧光显微镜进行吞噬性腹膜细胞迁移分析。

结果

在本研究中,我们观察到所有组的腹膜、肾脏、脾脏和肝脏样本中均存在 PKH+细胞。在感染的小鼠中,我们还在肺和脑中发现了 PKH+细胞。HH 状态并没有影响这个过程。

结论

在本研究中,我们观察到腹膜吞噬细胞迁移到白色念珠菌感染的组织中,HH 状态并没有干扰这个过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1820/3616899/36559008f9f9/1471-2334-13-147-1.jpg

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