Schoeler G B, Manweiler S A, Wikel S K
Department of Entomology and Plant Pathology, 127 Noble Research Center, Oklahoma State University, Stillwater, Oklahoma 74078, USA.
Parasite Immunol. 2000 Jan;22(1):31-40. doi: 10.1046/j.1365-3024.2000.00272.x.
Lyme borreliosis, caused by Borrelia burgdorferi, is transmitted by Ixodes scapularis in the eastern and midwestern United States and by Ixodes pacificus in the far-Western United States. Studies have shown that infestation with I. scapularis nymphs modulates host cytokine production; however, the influence of I. pacificus infestation on host cytokines remains uninvestigated. This study demonstrated how repeated infestations with pathogen-free I. scapularis or I. pacificus nymphs affects the production of the macrophage cytokines IL-1beta, IL-6 and tumour necrosis factor-alpha and the T lymphocyte cytokines IL-2, IL-4, IL-5, IL-6, IL-10 and IFN-gamma by C3H/HeN mice. Female mice were infested once or twice with pathogen-free I. scapularis or I. pacificus nymphs, with a 14-day tick-free period between exposures. After each infestation, tick biology parameters were assessed and macrophage and T lymphocyte cytokine production measured by antigen capture ELISA. Acquired resistance to tick feeding did not develop after infestation with either tick species. Differences in cytokine production were observed between infested and noninfested mice, and between mice infested with either I. scapularis or I. pacificus nymphs. Infestations polarized cytokine production towards a Th2 cytokine profile, with suppression of pro-inflammatory Th1 cytokines. This pattern of cytokine production is more pronounced for I. pacificus infested mice.
莱姆病疏螺旋体病由伯氏疏螺旋体引起,在美国东部和中西部地区通过肩突硬蜱传播,在远西部地区通过太平洋硬蜱传播。研究表明,感染肩突硬蜱若虫会调节宿主细胞因子的产生;然而,太平洋硬蜱感染对宿主细胞因子的影响仍未得到研究。本研究证明了用无病原体的肩突硬蜱或太平洋硬蜱若虫反复感染如何影响C3H/HeN小鼠巨噬细胞细胞因子白细胞介素-1β、白细胞介素-6和肿瘤坏死因子-α以及T淋巴细胞细胞因子白细胞介素-2、白细胞介素-4、白细胞介素-5、白细胞介素-6、白细胞介素-10和干扰素-γ的产生。雌性小鼠用无病原体的肩突硬蜱或太平洋硬蜱若虫感染一次或两次,两次感染之间有14天的无蜱期。每次感染后,评估蜱的生物学参数,并通过抗原捕获ELISA测量巨噬细胞和T淋巴细胞细胞因子的产生。用这两种蜱中的任何一种感染后,均未产生对蜱叮咬的获得性抗性。在感染和未感染的小鼠之间,以及在感染肩突硬蜱或太平洋硬蜱若虫的小鼠之间,观察到细胞因子产生的差异。感染使细胞因子产生向Th2细胞因子谱极化,同时促炎性Th1细胞因子受到抑制。这种细胞因子产生模式在太平洋硬蜱感染的小鼠中更为明显。