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在马里同域生活的儿童中,感染疟原虫后细胞因子、趋化因子和疟疾特异性抗体水平的变化。

Changes in the levels of cytokines, chemokines and malaria-specific antibodies in response to Plasmodium falciparum infection in children living in sympatry in Mali.

机构信息

Department of Immunology, Wenner-Gren Institute, Stockholm University, Svante Arrheniusväg 20C, 10691 Stockholm, Sweden.

出版信息

Malar J. 2012 Apr 5;11:109. doi: 10.1186/1475-2875-11-109.

DOI:10.1186/1475-2875-11-109
PMID:22480186
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3366880/
Abstract

BACKGROUND

The Fulani are known to be less susceptible to Plasmodium falciparum malaria as reflected by lower parasitaemia and fewer clinical symptoms than other sympatric ethnic groups. So far most studies in these groups have been performed on adults, which is why little is known about these responses in children. This study was designed to provide more information on this gap.

METHODS

Circulating inflammatory factors and antibody levels in children from the Fulani and Dogon ethnic groups were measured. The inflammatory cytokines; interleukin (IL)-1beta, IL-6, IL-8, IL-10, IL-12p70, tumor necrosis factor (TNF) and the chemokines; regulated on activation normal T cell expressed and secreted (RANTES), monokine-induced by IFN-gamma (MIG), monocyte chemotactic protein (MCP)-1 and IFN-gamma-inducible protein (IP)-10 were measured by cytometric bead arrays. The levels of interferon (IFN)-alpha, IFN-gamma and malaria-specific antibodies; immunoglobulin (Ig) G, IgM and IgG subclasses (IgG1-IgG4) were measured by ELISA.

RESULTS

The results revealed that the Fulani children had higher levels of all tested cytokines compared to the Dogon, in particular IFN-gamma, a cytokine known to be involved in parasite clearance. Out of all the tested chemokines, only MCP-1 was increased in the Fulani compared to the Dogon. When dividing the children into infected and uninfected individuals, infected Dogon had significantly lower levels of RANTES compared to their uninfected peers, and significantly higher levels of MIG and IP-10 as well as MCP-1, although the latter did not reach statistical significance. In contrast, such patterns were not seen in the infected Fulani children and their chemokine levels remained unchanged upon infection compared to uninfected counterparts. Furthermore, the Fulani also had higher titres of malaria-specific IgG and IgM as well as IgG1-3 subclasses compared to the Dogon.

CONCLUSIONS

Taken together, this study demonstrates, in accordance with previous work, that Fulani children mount a stronger inflammatory and antibody response against P. falciparum parasites compared to the Dogon and that these differences are evident already at an early age. The inflammatory responses in the Fulani were not influenced by an active infection which could explain why less clinical symptoms are seen in this group.

摘要

背景

富拉尼人被认为不易感染恶性疟原虫疟疾,其寄生虫血症和临床症状比其他同域族群少。到目前为止,这些族群的大多数研究都是在成年人中进行的,因此,人们对儿童的这些反应知之甚少。本研究旨在提供更多关于这一空白的信息。

方法

测量富拉尼族和多贡族儿童的循环炎症因子和抗体水平。通过流式细胞术珠阵列测量炎症细胞因子白细胞介素(IL)-1β、IL-6、IL-8、IL-10、IL-12p70、肿瘤坏死因子(TNF)和趋化因子调节活化正常 T 细胞表达和分泌(RANTES)、干扰素-γ诱导的单核细胞趋化蛋白(MIG)、单核细胞趋化蛋白-1(MCP-1)和γ干扰素诱导蛋白(IP)-10。通过 ELISA 测量干扰素(IFN)-α、IFN-γ和疟疾特异性抗体;免疫球蛋白(Ig)G、IgM 和 IgG 亚类(IgG1-IgG4)的水平。

结果

结果表明,与多贡族相比,富拉尼族儿童的所有测试细胞因子水平均较高,特别是 IFN-γ,这是一种已知参与寄生虫清除的细胞因子。在所测试的所有趋化因子中,只有 MCP-1 在富拉尼族中比多贡族增加。将儿童分为感染和未感染个体后,与未感染的同龄人相比,感染的多贡族的 RANTES 水平显著降低,而 MIG 和 IP-10 以及 MCP-1 的水平显著升高,尽管后者没有达到统计学意义。相比之下,在感染的富拉尼族儿童中没有出现这种模式,并且与未感染的同龄人相比,感染后的趋化因子水平保持不变。此外,与多贡族相比,富拉尼族的疟疾特异性 IgG 和 IgM 以及 IgG1-3 亚类的滴度也更高。

结论

总的来说,这项研究表明,与之前的工作一致,富拉尼族儿童对恶性疟原虫寄生虫的炎症和抗体反应比多贡族更强,而且这些差异在早期就已经很明显。富拉尼族的炎症反应不受活动性感染的影响,这可以解释为什么在该族群中观察到较少的临床症状。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc74/3366880/0f66285b24c2/1475-2875-11-109-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc74/3366880/2b820bdbeae6/1475-2875-11-109-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc74/3366880/01e4f31932f1/1475-2875-11-109-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc74/3366880/706798e65342/1475-2875-11-109-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc74/3366880/0f66285b24c2/1475-2875-11-109-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc74/3366880/2b820bdbeae6/1475-2875-11-109-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc74/3366880/01e4f31932f1/1475-2875-11-109-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc74/3366880/706798e65342/1475-2875-11-109-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc74/3366880/0f66285b24c2/1475-2875-11-109-4.jpg

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