Laboratoire du Paludisme, Institut Pasteur de Dakar, Dakar, Sénégal.
Infect Immun. 2012 Aug;80(8):2963-70. doi: 10.1128/IAI.00072-12. Epub 2012 Jul 2.
Recent studies suggest shared pathogenic pathways during malaria and allergy. Indeed, IgE, histamine, and the parasite-derived Plasmodium falciparum histamine-releasing factor translationally controlled tumor protein (PfTCTP) can be found at high levels in serum from patients experiencing malaria, but their relationship with basophil activation remains unknown. We recruited P. falciparum-infected patients in Senegal with mild malaria (MM; n = 19) or severe malaria (SM; n = 9) symptoms and healthy controls (HC; n = 38). Levels of serum IgE, PfTCTP, and IgG antibodies against PfTCTP were determined by enzyme-linked immunosorbent assays (ELISA). Basophil reactivities to IgE-dependent and -independent stimulations were measured ex vivo using fresh blood by looking at the expression level of the basophil activation marker CD203c with flow cytometry. Unstimulated basophils from MM had significantly lower levels of CD203c expression compared to those from HC and SM. After normalization on this baseline level, basophils from SM showed an enhanced reactivity to calcimycin (A23187) and hemozoin. Although SM reached higher median levels of activation after anti-IgE stimulation, great interindividual differences did not allow the results to reach statistical significance. When primed with recombinant TCTP before anti-IgE, qualitative differences in terms of a better ability to control excessive activation could be described for SM. IgE levels were very high in malaria patients, but concentrations in MM and SM were similar and were not associated with basophil responses, which demonstrates that the presence of IgE alone cannot explain the various basophil reactivities. Indeed, PfTCTP could be detected in 32% of patients, with higher concentrations for SM. These PfTCTP-positive patients displayed significantly higher basophil reactivities to any stimulus. Moreover, the absence of anti-PfTCTP IgG was associated with higher responses in SM but not MM. Our results show an association between basophil reactivity and malaria severity and suggest a pathogenic role for plasmodial PfTCTP in the induction of this allergy-like mechanism.
最近的研究表明,疟疾和过敏之间存在共同的致病途径。事实上,在经历疟疾的患者的血清中可以发现高水平的 IgE、组胺和寄生虫源性疟原虫裂殖体透明质酸酶转运蛋白(PfTCTP)以及疟原虫释放组胺的因子(Plasmodium falciparum histamine-releasing factor translationally controlled tumor protein,PfTCTP),但其与嗜碱性粒细胞活化的关系尚不清楚。我们招募了塞内加尔患有轻度疟疾(MM;n=19)或重度疟疾(SM;n=9)症状的疟原虫感染患者和健康对照者(HC;n=38)。通过酶联免疫吸附试验(ELISA)测定血清 IgE、PfTCTP 和针对 PfTCTP 的 IgG 抗体水平。通过使用新鲜血液进行体外测量,通过流式细胞术观察嗜碱性粒细胞活化标志物 CD203c 的表达水平,来测量 IgE 依赖性和非依赖性刺激物对嗜碱性粒细胞的反应性。与 HC 和 SM 相比,MM 患者的未刺激嗜碱性粒细胞 CD203c 表达水平明显降低。在这个基线水平上进行归一化后,SM 的嗜碱性粒细胞对钙调霉素(A23187)和血影蛋白的反应性增强。尽管在抗 IgE 刺激后,SM 达到了更高的平均激活水平,但个体之间的巨大差异使得结果无法达到统计学意义。当在用抗 IgE 预刺激时用重组 TCTP 进行预刺激时,SM 可以描述为在控制过度激活方面具有更好的能力的定性差异。疟疾病例患者的 IgE 水平非常高,但 MM 和 SM 的浓度相似,且与嗜碱性粒细胞反应无关,这表明仅存在 IgE 不能解释各种嗜碱性粒细胞反应性。事实上,在 32%的患者中可以检测到 PfTCTP,SM 的浓度更高。这些 PfTCTP 阳性患者对任何刺激的嗜碱性粒细胞反应性明显更高。此外,在 SM 中但不在 MM 中,缺乏抗 PfTCTP IgG 与更高的反应性相关。我们的结果表明,嗜碱性粒细胞反应性与疟疾严重程度之间存在关联,并提示疟原虫 PfTCTP 在诱导这种类似过敏的机制中的致病作用。