The protective effect of Helicobacter Pylori infection on the susceptibility of multiple sclerosis

The protective effect of Helicobacter Pylori infection on the susceptibility of multiple sclerosis
复制标题

DOI:
10.1016/j.jneuroim.2019.577069
复制
发表时间:
2019-12-15
影响因子:
3.3
通讯作者:
Jalilian, Farid Azizi
Jalilian, Farid Azizi
中科院分区:
医学4区
文献类型:
--
作者:
Ranjbar, Reza;Karampoor, Sajad;Jalilian, Farid Azizi

文献摘要

被引文献

相似文献

近年来,幽门螺杆菌(Hp)对自身免疫性疾病的可能的保护作用已被报道在多发性硬化症(MS)的实验小鼠模型,并有限制的相互矛盾的流行病学数据有关Hp血清学在MS患者。本研究旨在确定MS患者中Hp的血清阳性率,然后调查HP感染的MS患者和血清阴性MS患者的促/抗炎细胞因子水平。387例MS患者纳入研究,并根据性别和年龄调整为420例健康受试者。用酶联免疫吸附试验(ELISA)测定抗H. pylori感染。在血清阳性/血清阴性MS患者和健康个体中评价了一些促炎/抗炎细胞因子水平。结果表明,MS患者HP血清阳性率明显低于健康人(P <0.0001)。此外,我们发现HP血清阳性MS患者与血清阴性MS患者相比,扩展残疾状态量表(EDSS)较低(P <0.011)。此外,我们还阐明了HP感染的MS患者的促炎细胞因子水平(包括IFN-γ、TNF-α、IL-6和IL-17)低于血清阴性MS患者。HP感染的MS患者血清中IL-4、IL-10水平明显高于HP阴性的MS患者。在这项研究中,我们表明,HP感染与MS呈负相关,可以想象,可能作为一种保护剂对MS的这种保护作用背后的确切机制仍然难以捉摸。但HP可能通过调节细胞因子信号通路参与MS的发病过程。
In recent years, a possible protective role of Helicobacter pylori (Hp) against autoimmune disease has been reported in an experimental murine model of multiple sclerosis (MS), and there are restricted conflicting epidemiologic data concerning Hp serology in MS patients. This study was aimed to determine the seroprevalence of Hp in MS patients and then investigates pro/anti-inflammatory cytokine levels in MS patients infected with HP and seronegative MS patients. Three hundred eighty-seven patients with MS were included in the study and were adjusted by gender and age to 420 healthy subjects. An enzyme-linked immunoassay (ELISA) was used to determine the presence of specific IgG antibodies against H. pylori in the serum sample of both groups. Some pro/anti-inflammatory cytokines levels were evaluated in seropositive/seronegative MS patients and healthy individuals. Our result showed that in patients with MS HP seropositivity was significantly lower than the healthy individual (P < .0001). Also, we showed that HP seropositive MS patients had lower Expanded Disability Status Scale (EDSS) when compared with seronegative MS patients (P < .011). Moreover, we illustrated that proinflammatory cytokine levels include IFN-gamma, TNF-alpha, IL-6, and IL-17 in MS patients infected with HP were lower than seronegative MS patients. Besides, the levels of anti-inflammatory cytokines include IL-4 and IL-10 was significantly higher in MS patients infected with HP when compared with MS patients seronegative for HP infection. In this study, we indicated that HP infection negatively correlated with MS, and conceivably may act as a protective agent against MS. The precise mechanism behind this protective effect remains elusive. However, it seems HP can modulate cytokine signaling, which involved in MS pathogenesis.