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血清中寄生虫负荷、低水平的 IL-33 或 TNF-α 和高水平的 IL-10 可调节人体过敏反应。

Modulation of Allergic Reactivity in Humans Is Dependent on Parasite Burden, Low Levels of IL-33 or TNF-α and High Levels of IL-10 in Serum.

机构信息

Department of Parasitology, Federal University of Minas Gerais (UFMG), Belo Horizonte, Brazil.

Schistosomiasis Laboratory, René Rachou Research Center, Oswaldo Cruz Foundation, Belo Horizonte, Brazil.

出版信息

Front Immunol. 2019 Jan 18;9:3158. doi: 10.3389/fimmu.2018.03158. eCollection 2018.

DOI:10.3389/fimmu.2018.03158
PMID:30713536
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6345678/
Abstract

Helminth infections and allergies are characterized by a predominant type-2 immune response. In schistosomiasis, the Th-2 response is usually accompanied by induction of immunoregulatory mechanisms that contribute to worm survival and less severe schistosomiasis. Although helminth-induced immunomodulatory mechanisms seem to affect atopy, epidemiological studies on the relationship between helminths and allergy have been inconsistent, and data suggest that the modulatory effects may be influenced by helminth species, chronicity of infection, and parasite burden. Here we performed a cross-sectional study to investigate the effects of parasite burden and immune response on allergic reactivity of individuals living in a schistosomiasis endemic area in Brazil. Fecal samples from the participants were collected for extensive parasitological examinations by spontaneous sedimentation, Kato-Katz, Helmintex and Saline Gradient tests and molecular detection of by qPCR. Additionally, the concentrations of cytokines and chemokines, total IgE and IgE-reactivity to common house dust allergens were quantified from serum samples. IgE reactivity to dust allergens was detected in 47 individuals (23.8%), and 140 individuals (54.4%) were diagnosed with infection. Most of the infected population (108 individuals) presented very low parasite burden (≤12 eggs/g of feces). The frequency and intensity ( ≤ 0.03) of allergic reactivity were lower in infected compared with non-infected individuals. Multivariable logistic regression models adjusted by age revealed that allergic reactivity was positively associated with low IL-10 response (OR, 4.55, 95% CI, 0.56-7.36) and high concentration of the inflammatory mediators IL-33 (OR, 2.70, 95% CI, 1.02-7.15) or TNF-α (OR, 6.88, 95% CI, 0.32-143.39) in serum, and inversely associated with infection (OR, 0.38, 95% CI, 0.16-0.87). Most importantly, the logistic regression demonstrated that the modulatory effects of infection depend on parasite burden, with individuals infected with ≤12 eggs/g of feces showing allergic IgE-reactivity similar to non-infected individuals Altogether, our data show that immunomodulation of allergic reactivity depends on burden, low type-2 inflammatory response, and high level of IL-10.

摘要

寄生虫感染和过敏的特点是 2 型免疫反应占主导地位。在血吸虫病中,Th2 反应通常伴随着免疫调节机制的诱导,这有助于蠕虫的存活和减轻血吸虫病的严重程度。尽管寄生虫诱导的免疫调节机制似乎会影响过敏,但寄生虫和过敏之间关系的流行病学研究一直不一致,并且数据表明,调节作用可能受到寄生虫种类、感染的慢性程度和寄生虫负担的影响。在这里,我们进行了一项横断面研究,以调查寄生虫负担和免疫反应对生活在巴西血吸虫病流行地区的个体过敏反应的影响。从参与者的粪便样本中采集了大量寄生虫,通过自然沉淀、加藤氏法、Helmintex 和盐水梯度试验以及 qPCR 进行了广泛的寄生虫学检查。此外,还从血清样本中定量了细胞因子和趋化因子、总 IgE 和 IgE 对常见屋尘过敏原的反应性。在 47 名个体(23.8%)中检测到对尘螨过敏原的 IgE 反应性,140 名个体(54.4%)被诊断患有 感染。大多数感染人群(108 人)的寄生虫负担非常低(≤12 个卵/克粪便)。与未感染者相比,感染者的过敏反应频率和强度(≤0.03)较低。多变量逻辑回归模型通过年龄调整后显示,过敏反应与低 IL-10 反应(OR,4.55,95%CI,0.56-7.36)和血清中炎症介质 IL-33(OR,2.70,95%CI,1.02-7.15)或 TNF-α(OR,6.88,95%CI,0.32-143.39)浓度高呈正相关,与 感染呈负相关(OR,0.38,95%CI,0.16-0.87)。最重要的是,逻辑回归表明,感染的调节作用取决于寄生虫负担,感染≤12 个卵/克粪便的个体的过敏 IgE 反应与未感染者相似。综上所述,我们的数据表明,过敏反应的免疫调节取决于寄生虫负担、低 2 型炎症反应和高水平的 IL-10。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c38/6345678/612bd93c30b4/fimmu-09-03158-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c38/6345678/435da423b30b/fimmu-09-03158-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c38/6345678/6ff91ffe2004/fimmu-09-03158-g0002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c38/6345678/612bd93c30b4/fimmu-09-03158-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c38/6345678/435da423b30b/fimmu-09-03158-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c38/6345678/6ff91ffe2004/fimmu-09-03158-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c38/6345678/af90564f8122/fimmu-09-03158-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c38/6345678/dbdcff73de2a/fimmu-09-03158-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c38/6345678/612bd93c30b4/fimmu-09-03158-g0005.jpg

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