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利什曼原虫感染会破坏白蛉传播媒介的摄食机制,并通过叮咬实现寄生虫传播。

Leishmania infections damage the feeding mechanism of the sandfly vector and implement parasite transmission by bite.

作者信息

Schlein Y, Jacobson R L, Messer G

机构信息

Department of Parasitology, Hebrew University, Hadassah Medical School, Jersalem, Israel.

出版信息

Proc Natl Acad Sci U S A. 1992 Oct 15;89(20):9944-8. doi: 10.1073/pnas.89.20.9944.

Abstract

Leishmania parasites are transmitted by the bites of infected female sandflies by a mechanism that has not been clarified. Leishmania infections in the vector develop only in the gut, and the parasites' exit is through the food channel in the proboscis. The problem is how during the bite, when blood flows in, parasites are emitted through the same channel in the opposite direction. It is well documented that infected sandflies maintained on sugar diets are potent vectors, whereas transmission fails after constant feeding on blood. Hence to study the mechanism of transmission, we fed these diets to Phlebotomus papatasi infected with L. major. Histological examination demonstrated that only in the sugar-fed flies did the cuticle lining of the cardiac valve detach and other valve tissues degenerate gradually. The injury of the main valve of the food pumps hindered gorging of most flies when force-fed from capillaries, and they regurgitated the gut contents with fluids from the capillaries. We suggest that infections are caused by parasites regurgitated from the stomach that are deposited in the host tissue. We found that secretion of chitinolytic enzymes by cultured L. major parasites is inhibited by blood or hemoglobin, and hence these enzymes are apparently absent from the blood-fed infected flies, where the cardiac valve appears undamaged. We therefore presume that lysis of the chitin in the cuticle lining of the valve leads to exposure and degeneration of the underlying tissues.

摘要

利什曼原虫通过尚未明确的机制由受感染的雌性白蛉叮咬传播。利什曼原虫在媒介昆虫体内仅在肠道内发育,寄生虫通过口器中的食物通道排出。问题在于在叮咬过程中,当血液流入时,寄生虫如何通过同一通道向相反方向排出。有充分的文献记载,以糖为食的受感染白蛉是有效的传播媒介,而持续以血为食后传播就会失败。因此,为了研究传播机制,我们将这些食物喂给感染了硕大利什曼原虫的巴氏白蛉。组织学检查表明,只有在以糖为食的白蛉中,心瓣膜的角质层衬里才会分离,其他瓣膜组织也会逐渐退化。当用毛细管强行喂食时,食物泵主瓣膜的损伤阻碍了大多数白蛉的饱食,它们会将肠道内容物与毛细管中的液体一起反流出来。我们认为感染是由从胃中反流出来并沉积在宿主组织中的寄生虫引起的。我们发现,培养的硕大利什曼原虫分泌的几丁质酶会受到血液或血红蛋白的抑制,因此在以血为食的受感染白蛉中显然不存在这些酶,在这些白蛉中的心瓣膜看起来没有受损。因此我们推测,瓣膜角质层衬里中的几丁质溶解会导致其下组织的暴露和退化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e090/50250/a557cf156978/pnas01094-0589-a.jpg

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