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Histamine Released From Skin-Infiltrating Basophils but Not Mast Cells Is Crucial for Acquired Tick Resistance in Mice

机译:组胺从浸润皮肤的嗜碱性粒细胞释放但不是肥大细胞对于小鼠获得的抗ick虱病至关重要

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摘要

Ticks are blood-feeding arthropods that can transmit pathogens to humans and animals, leading to serious infectious diseases such as Lyme disease. After single or multiple tick infestation, some animal species develop resistance to tick feeding, leading to reduced risk of pathogen transmission. In mice infested with larval Haemaphysalis longicornis ticks, both mast cells and basophils reportedly play key roles in the manifestation of acquired tick resistance (ATR), but it remains ill-defined how they contribute to it. Here, we investigated their products responsible for ATR. Treatment of mice with antihistamine abolished the ATR while histamine or histamine H1 receptor agonist reduced tick-feeding even in the first infestation. In accordance with these, mice deficient for histamine production showed little or no ATR, indicating the crucial role for histamine in the expression of ATR. Adoptive transfer of mast cells and basophils derived from histamine-sufficient or deficient mice to recipient mice lacking mast cells and basophils, respectively, revealed that histamine produced by basophils but not mast cells is essential for the manifestation of ATR, in contrast to the case of local and systemic anaphylaxis where mast cell-derived histamine is the major player. During the second but not first tick infestation, basophils accumulated and made a cluster, surrounding a tick mouthpart, in the epidermis whereas mast cells were scattered and localized mainly in the dermis, more distantly from a tick mouthpart. This appears to explain why basophil-derived histamine is much more effective than mast cell-derived one. Histamine-sufficient, but not -deficient mice showed the thickened epidermis at the second tick-feeding site. Taken together, histamine released from skin-infiltrating basophils rather than skin-resident mast cells plays a crucial role in the manifestation of ATR, perhaps through promotion of epidermal hyperplasia that may inhibit tick feeding.
机译:cks虫是食血的节肢动物,可以将病原体传播给人类和动物,导致严重的传染病,例如莱姆病。一次或多次tick虫侵染后,某些动物对tick食产生抵抗力,从而降低了病原体传播的风险。据报道,在感染了幼虫血红tick虫的小鼠中,肥大细胞和嗜碱性粒细胞在获得性tick虫抗性(ATR)的表现中均起着关键作用,但仍不清楚如何发挥其作用。在这里,我们调查了负责ATR的产品。用抗组胺药治疗的小鼠消除了ATR,而组胺或组胺H1受体激动剂甚至在第一次感染时也减少了tick的进食。据此,组胺产生缺陷的小鼠显示很少或没有ATR,表明组胺在ATR表达中的关键作用。分别将来自组胺充足或不足组小鼠的肥大细胞和嗜碱性粒细胞分别过继转移至缺乏肥大细胞和嗜碱粒细胞的受体小鼠中,表明嗜碱性粒细胞而非肥大细胞产生的组胺对于ATR的表现是必不可少的。局部和全身过敏反应,其中肥大细胞衍生的组胺是主要因素。在第二次但不是第一次的tick虫感染期间,嗜碱性粒细胞在表皮周围聚集并形成簇,围绕,嘴部,而肥大细胞则主要在真皮中散布和定位,离a嘴部较远。这似乎可以解释为什么嗜碱性粒细胞来源的组胺比肥大细胞来源的组胺更有效。组胺充足但不是不足的小鼠在第二个tick喂养部位显示表皮增厚。两者合计,从渗透皮肤的嗜碱性粒细胞而不是驻留皮肤的肥大细胞释放的组胺在ATR的表现中起着至关重要的作用,也许是通过促进可能抑制tick食的表皮增生。

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