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血吸虫病诱导的肺血管重塑中炎症细胞谱增强

Enhanced inflammatory cell profiles in schistosomiasis-induced pulmonary vascular remodeling.

作者信息

Ali Zahara, Kosanovic Djuro, Kolosionek Ewa, Schermuly Ralph T, Graham Brian B, Mathie Alistair, Butrous Ghazwan

机构信息

University of Kent, Medway School of Pharmacy, Chatham, Kent, UK.

Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Center for Lung Research (DZL), Giessen, Germany.

出版信息

Pulm Circ. 2017 Apr 4;7(1):244-252. doi: 10.1086/690687. eCollection 2017 Mar.

Abstract

Schistosomiasis (bilharzia) is a neglected parasitic disease caused by trematode flatworms of the genus which affects over 240 million people worldwide. It is characterized by the formation of inflammatory granulomas around deposited parasite eggs. Recent studies have revealed that immune and inflammatory responses play a crucial role in pathogenesis of schistosomiasis. The aim of this paper is to systematically evaluate the number and distribution of inflammatory cells in -infected mice at different doses and time points. Immunohistochemistry was performed on lung and liver tissue sections from -infected mice and uninfected healthy controls. Positively stained cells in whole-lung/liver tissue sections, surrounding the eggs, and in the different compartments of the tissues, were counted. We found a significant increase in the number of mast cells (toluidine blue), CD3 cells, CD14 cells, CD68 cells, and CD15 cells in -infected tissues compared with untreated healthy controls ( ≤ 0.05 for all). Our findings revealed altered and enhanced immune cell infiltration in schistosomiasis. We suggest that these cells may contribute to the pathophysiology of resulting in pulmonary vascular remodeling.

摘要

血吸虫病是一种由血吸虫属吸虫纲扁形虫引起的被忽视的寄生虫病,全球有超过2.4亿人受其影响。其特征是在沉积的寄生虫卵周围形成炎性肉芽肿。最近的研究表明,免疫和炎症反应在血吸虫病的发病机制中起关键作用。本文的目的是系统评估不同剂量和时间点感染小鼠体内炎性细胞的数量和分布。对感染小鼠和未感染的健康对照的肺和肝组织切片进行免疫组织化学分析。对全肺/肝组织切片、虫卵周围以及组织不同区域中阳性染色的细胞进行计数。我们发现,与未处理的健康对照相比,感染组织中肥大细胞(甲苯胺蓝染色)、CD3细胞、CD14细胞、CD68细胞和CD15细胞的数量显著增加(所有P≤0.05)。我们的研究结果显示血吸虫病中免疫细胞浸润发生改变且增强。我们认为这些细胞可能参与导致肺血管重塑的病理生理过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/65e3/5448541/2a777a84291c/10.1086_690687-fig1.jpg

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