Anderson Jennifer M, Moore Ian N, Nagata Bianca M, Ribeiro José M C, Valenzuela Jesus G, Sonenshine Daniel E
Vector Biology Section, Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases (NIH), Rockville, MD, United States.
Infectious Disease and Pathogenesis Section, Comparative Medicine Branch, National Institute of Allergy and Infectious Diseases (NIH), Rockville, MD, United States.
Front Immunol. 2017 Dec 18;8:1784. doi: 10.3389/fimmu.2017.01784. eCollection 2017.
Ticks transmit infectious agents including bacteria, viruses and protozoa. However, their transmission may be compromised by host resistance to repeated tick feeding. Increasing host resistance to repeated tick bites is well known in laboratory animals, including intense inflammation at the bite sites. However, it is not known whether this also occurs in wild rodents such as white-footed mice, , and other wildlife, or if it occurs at all. According to the "host immune incompetence" hypothesis, if these mice do not have a strong inflammatory response, they would not reject repeated tick bites by . To test this hypothesis, histopathological studies were done comparing dermal inflammation in versus guinea pigs, , repeatedly infested with . In , the immune cell composition was like that seen in laboratory mouse models, with some differences. However, there was a broad sessile lesion with intact dermal architecture, likely enabling the ticks to continue feeding unimpeded. In contrast, in , there was a relatively similar mixed cellular profile, but there also was a large, leukocyte-filled cavitary lesion and scab-like hyperkeratotic changes to the epidermal layer, along with itching and apparent pain. Ticks attached to sensitized fed poorly or were dislodged, presumably due to the weakened anchoring of the tick's mouthparts cemented in the heavily inflamed and disintegrating dermal tissues. This is the first time that the architecture of the skin lesions has been recognized as a major factor in understanding tick-host tolerance versus tick bite rejection. These findings broadly strengthen previous work done on lab animal models but also help explain why can repeatedly parasitize white-footed mice, supporting the "immune evasion theory" but cannot repeatedly parasitize other, non-permissive hosts such as guinea pigs.
蜱虫传播包括细菌、病毒和原生动物在内的传染因子。然而，宿主对蜱虫反复叮咬的抵抗力可能会影响它们的传播。在实验动物中，提高宿主对蜱虫反复叮咬的抵抗力是众所周知的，包括叮咬部位出现强烈炎症。然而，尚不清楚这种情况是否也发生在诸如白足鼠等野生啮齿动物以及其他野生动物身上，或者是否真的会发生。根据“宿主免疫无能”假说，如果这些小鼠没有强烈的炎症反应，它们就不会排斥蜱虫的反复叮咬。为了验证这一假说，进行了组织病理学研究，比较了白足鼠和豚鼠在反复感染蜱虫后的皮肤炎症情况。在白足鼠身上，免疫细胞组成与实验室小鼠模型中的情况相似，但也存在一些差异。然而，有一个广泛的无柄病变，真皮结构完整，这可能使蜱虫能够继续不受阻碍地进食。相比之下，在豚鼠身上，有相对相似的混合细胞特征，但也有一个大的、充满白细胞的空洞性病变以及表皮层的痂状角化过度变化，同时伴有瘙痒和明显疼痛。附着在致敏豚鼠身上的蜱虫进食不佳或被驱赶，可能是由于蜱虫口器固定在严重发炎和分解的真皮组织中导致的锚固力减弱。这是首次认识到皮肤病变的结构是理解蜱虫 - 宿主耐受性与蜱虫叮咬排斥反应的一个主要因素。这些发现广泛地强化了先前在实验动物模型上所做的工作，但也有助于解释为什么蜱虫能够反复寄生于白足鼠，支持了“免疫逃避理论”，但不能反复寄生于其他非适宜宿主，如豚鼠。
