Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, Maryland, United States of America.
PLoS Negl Trop Dis. 2012;6(12):e1970. doi: 10.1371/journal.pntd.0001970. Epub 2012 Dec 20.
Chronic helminth infections induce a Th2 immune shift and establish an immunoregulatory milieu. As both of these responses can suppress Th1 immunity, which is necessary for control of Mycobacterium tuberculosis (MTB) infection, we hypothesized that chronic helminth infections may exacerbate the course of MTB.
METHODOLOGY/PRINCIPAL FINDINGS: Co-infection studies were conducted in cotton rats as they are the natural host for the filarial nematode Litomosoides sigmodontis and are an excellent model for human MTB. Immunogical responses, histological studies, and quantitative mycobacterial cultures were assessed two months after MTB challenge in cotton rats with and without chronic L. sigmodontis infection. Spleen cell proliferation and interferon gamma production in response to purified protein derivative were similar between co-infected and MTB-only infected animals. In contrast to our hypothesis, MTB loads and occurrence and size of lung granulomas were not increased in co-infected animals.
CONCLUSIONS/SIGNIFICANCE: These findings suggest that chronic filaria infections do not exacerbate MTB infection in the cotton rat model. While these results suggest that filaria eradication programs may not facilitate MTB control, they indicate that it may be possible to develop worm-derived therapies for autoimmune diseases that do not substantially increase the risk for infections.
慢性寄生虫感染会引起 Th2 免疫偏移，并建立免疫调节环境。由于这两种反应都可能抑制 Th1 免疫，而 Th1 免疫对于控制结核分枝杆菌（MTB）感染是必要的，因此我们假设慢性寄生虫感染可能会加重 MTB 的病程。
方法/主要发现：在棉鼠中进行了共感染研究，因为它们是旋尾丝虫的天然宿主，并且是人类 MTB 的优秀模型。在 MTB 感染棉鼠两个月后，评估了有和没有慢性 L. sigmodontis 感染的棉鼠中的免疫反应、组织学研究和定量分枝杆菌培养。在共感染和 MTB 单独感染的动物中，对纯化蛋白衍生物的脾细胞增殖和干扰素γ产生相似。与我们的假设相反，在共感染的动物中，MTB 负荷和肺肉芽肿的发生和大小并没有增加。
结论/意义：这些发现表明，慢性丝虫感染不会加重棉鼠模型中的 MTB 感染。虽然这些结果表明，消灭丝虫的计划可能不会促进 MTB 的控制，但它们表明，为自身免疫性疾病开发源自蠕虫的治疗方法可能不会显著增加感染的风险。
