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与慢性疟疾暴露相关的肝脾肿大:血吸虫病加剧的促炎机制的证据。

Hepatosplenomegaly associated with chronic malaria exposure: evidence for a pro-inflammatory mechanism exacerbated by schistosomiasis.

作者信息

Wilson S, Jones F M, Mwatha J K, Kimani G, Booth M, Kariuki H C, Vennervald B J, Ouma J H, Muchiri E, Dunne D W

机构信息

Department of Pathology, University of Cambridge, Cambridge, UK.

出版信息

Parasite Immunol. 2009 Feb;31(2):64-71. doi: 10.1111/j.1365-3024.2008.01078.x.

DOI:10.1111/j.1365-3024.2008.01078.x
PMID:19149774
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2680340/
Abstract

In sub-Saharan Africa, chronic hepatosplenomegaly, with palpable firm/hard organ consistency, is common, particularly among school-aged children. This morbidity can be caused by long-term exposure to malaria, or by Schistosoma mansoni, and it is exacerbated when these two occur together. Although immunological mechanisms probably underlie the pathogenic process, these mechanisms have not been identified, nor is it known whether the two parasites augment the same mechanisms or induce unrelated processes that nonetheless have additive or synergistic effects. Kenyan primary schoolchildren, living in a malaria/schistosomiasis co-transmission area, participated in cross-sectional parasitological and clinical studies in which circulating immune modulator levels were also measured. Plasma IL-12p70, sTNF-RII, IL-10 and IL-13 levels correlated with relative exposure to malaria, and with hepatosplenomegaly. Soluble-TNF-RII and IL-10 were higher in children infected with S. mansoni. Hepatosplenomegaly caused by chronic exposure to malaria was clearly associated with increased circulating levels of pro-inflammatory mediators, with higher levels of regulatory modulators, and with tissue repair cytokines, perhaps being required to control the inflammatory response. The higher levels of regulatory modulators amongst S. mansoni infected children, compared to those without detectable S. mansoni and malarial infections, but exposed to malaria, suggest that S. mansoni infection may augment the underlying inflammatory reaction.

摘要

在撒哈拉以南非洲地区,慢性肝脾肿大很常见,肝脏质地坚硬可触及,在学龄儿童中尤为如此。这种病症可能由长期接触疟疾或曼氏血吸虫引起,当这两种病原体同时出现时病情会加重。尽管免疫机制可能是致病过程的基础,但这些机制尚未明确,也不清楚这两种寄生虫是增强相同的机制,还是引发虽不相关但具有累加或协同效应的过程。生活在疟疾/血吸虫病共同传播地区的肯尼亚小学生参与了横断面寄生虫学和临床研究,其中还测量了循环免疫调节剂水平。血浆白细胞介素-12p70、可溶性肿瘤坏死因子受体II(sTNF-RII)、白细胞介素-10和白细胞介素-13水平与疟疾的相对暴露程度以及肝脾肿大相关。感染曼氏血吸虫的儿童中可溶性肿瘤坏死因子受体II和白细胞介素-10水平较高。长期接触疟疾导致的肝脾肿大显然与促炎介质循环水平升高、调节性介质水平升高以及组织修复细胞因子有关,或许这些是控制炎症反应所必需的。与未检测到曼氏血吸虫感染但暴露于疟疾的儿童相比,感染曼氏血吸虫的儿童中调节性介质水平较高,这表明曼氏血吸虫感染可能会增强潜在的炎症反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c14/2680340/c724d8ef5870/pim0031-0064-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c14/2680340/b9a768c0321b/pim0031-0064-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c14/2680340/7048dfdd4634/pim0031-0064-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c14/2680340/c724d8ef5870/pim0031-0064-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c14/2680340/b9a768c0321b/pim0031-0064-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c14/2680340/7048dfdd4634/pim0031-0064-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c14/2680340/c724d8ef5870/pim0031-0064-f3.jpg

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