Contribution of the vibrio parahaemolyticus chromosome I type III secretion system to colonization of the Pacific oyster, crassostrea gigas

副溶血性弧菌是因食用生的或未煮熟的贝类而引起肠胃炎的重要原因。副溶血性弧菌在双壳类无脊椎动物中积聚，特别是牡蛎和贻贝。在副溶血性弧菌分离株中存在大量的多样性，并且毒性所需因子的数量尚未得到很好的了解。副溶血弧菌在成年牡蛎中不会引起疾病，被认为是牡蛎正常菌群的一部分。副溶血性弧菌基因组编码两个III型分泌系统。III型分泌系统是革兰氏阴性菌利用多蛋白复合物将蛋白质直接注入宿主细胞。它们通常存在于动植物病原体中，被认为是重要的毒力因子。令人惊讶的是，我们实验室的数据表明，III型分泌系统之一CI-T3SS在疾病相关和环境分离株中都有发现。这使我们假设CI-T3SS参与了牡蛎的定植和生存。在本文中，我们研究了副溶血性弧菌与牡蛎免疫系统之间的相互作用。与宿主密切相关的细菌需要避免被免疫系统识别为外来物。牡蛎的免疫系统由被称为血细胞的吞噬细胞组成。我们的数据表明，副溶血性弧菌逃避吞噬作用，这可以使它在牡蛎中存活。因此，我们将研究CI-T3SS是否在避免吞噬中起作用。第二个目标是确定CI-T3SS是否需要牡蛎的持久定植。总的来说，这些研究将使我们更好地了解副溶血性弧菌的海洋生活方式。由于副溶血性弧菌的毒力尚不明确，因此在牡蛎上市前清除副溶血性弧菌的方法是降低疾病风险的重要策略。了解副溶血性弧菌如何在牡蛎中持续存在将提高我们开发这些工具的能力。

Vibrio parahaemolyticus is a significant cause of gastroenteritis resulting from the consumption of raw or undercooked shellfish. V. parahaemolyticus accumulates in bivalve invertebrates, particularly oysters and mussels. There is a large amount of diversity within V. parahaemolyticus isolates, and the aresenal of factors required for virulence is not well understood. V. parahaemolytics does not cause disease in adult oysters, and is thought to be part of the oyster normal flora. The V. parahaemolyticus genome encodes two type III secretion systems. Type III secretion systems are mult-protein complexes used by Gram negative bacteria to inject proteins directly into the host cell. They are commonly found in animal and plant pathogens, and are considered important virulence factors. Surprisingly, data from our lab indicates that one of the type III secretion systems, the CI-T3SS, is found in both disease-associated and environmental isolates. This led us to hypothesize that the CI-T3SS is involved in colonization and survival within oysters. In this proposal, we examine the interaction between V. parahaemolyticus and the oyster immune system. Bacteria that live in close association with a host need to avoid recognition as foreign by the immune system. The oyster immune system is comprised of phagocytic cells called hemocytes. Our data suggests that V. parahaemolyticus evades phagocytosis, which could enable it to survive within the oyser. We will therefore examine whether the CI-T3SS plays a role in avoiding phagocytosis. A second aim is to determine whether the CI-T3SS is required for persistent colonization of the oyster. Collectively, these studies will allow us to better understand the marine lifestyle of V. parahaemolyticus. As virulence in V. parahaemolyticus is not well defined, methods for eliminating V. parahaemolyticus from oysters before they go to market is an important strategy to decrease the risk of disease. Understanding how V. parahaemolyticus persists in oysters will enhance our ability to develop these tools.