Kim Yonggyun, Ji Dongjin, Cho Sunghwan, Park Youngjin
Department of Agricultural Biology, College of Natural Sciences, Andong National University, Andong 760-749, Korea.
J Invertebr Pathol. 2005 Jul;89(3):258-64. doi: 10.1016/j.jip.2005.05.001.
Photorhabdus and Xenorhabdus are two genera of entomopathogenic bacteria having a mutualistic relationship with their respective nematode hosts, Heterorhabditis and Steinernema. One of the pathogenic mechanisms of these bacteria includes host immunodepression, which leads to lethal septicemia. It has been known that X. nematophila inhibits phospholipase A2 (PLA2) to induce host immunodepression. Here, we tested the hypothesis of PLA2 inhibition using another bacterial species involved in other genera. P. temperata subsp. temperata is the intestinal symbiont of an entomopathogenic nematode, H. megidis. The bacteria caused potent pathogenicity in a dose-dependent manner against the fifth instar larvae of a test target insect, Spodoptera exigua, as early as 24 h after the intra-hemocoelic injection. In response to the live bacterial injection, hemocyte nodulation (a cellular immune response) and prophenoloxidase (pPO) activation were inhibited, while the injection of heat-killed bacteria significantly induced both immune reactions. The immunodepression induced by the live bacteria was reversed by the addition of arachidonic acid, the catalytic product of phospholipase A2. In contrast, the addition of dexamethasone, a specific PLA2 inhibitor to the heat-killed bacterial treatment, inhibited both immune capacities. In addition to a previously known PLA2 inhibitory action of X. nematophila, the inhibition of P. temperata temperata on PLA2 suggests that bacteria symbiotic to entomopathogenic nematodes share a common pathogenic target to result in an immunodepressive state of the infected insects. To prove this generalized hypothesis, we used other bacterial species (X. bovienni, X. poinarii, and P. luminescens) involved in these two genera. All our experiments clearly showed that these other bacteria also share their inhibitory action against PLA2 to induce host immunodepression.
光杆状菌属和异小杆状菌属是两类昆虫病原细菌，它们与其各自的线虫宿主——异小杆线虫属和斯氏线虫属存在共生关系。这些细菌的致病机制之一包括宿主免疫抑制，这会导致致命的败血症。已知嗜线虫异小杆状菌会抑制磷脂酶A2（PLA2）以诱导宿主免疫抑制。在此，我们使用另一个属的细菌物种来检验PLA2抑制的假说。温和光杆状菌温带亚种是昆虫病原线虫大卵异小杆线虫的肠道共生菌。早在血腔注射后24小时，该细菌就以剂量依赖的方式对受试靶标昆虫甜菜夜蛾的五龄幼虫产生了强大的致病性。响应活菌注射，血细胞结节形成（一种细胞免疫反应）和前酚氧化酶（pPO）激活受到抑制，而注射热灭活细菌则显著诱导了这两种免疫反应。添加磷脂酶A2的催化产物花生四烯酸可逆转活菌诱导的免疫抑制。相反，向热灭活细菌处理中添加地塞米松（一种特异性PLA2抑制剂）会抑制这两种免疫能力。除了嗜线虫异小杆状菌先前已知的PLA2抑制作用外，温和光杆状菌温带亚种对PLA2的抑制表明，与昆虫病原线虫共生的细菌共享一个共同的致病靶点，从而导致被感染昆虫处于免疫抑制状态。为了证明这一普遍假说，我们使用了这两个属中的其他细菌物种（博维异小杆状菌、波氏异小杆状菌和发光光杆状菌）。我们所有的实验都清楚地表明，这些其他细菌也具有对PLA2的抑制作用，以诱导宿主免疫抑制。
