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Involvement of a tachylectin-like gene and its protein in pathogenesis of acute hepatopancreatic necrosis disease (AHPND) in the shrimp, Penaeus monodon
Program in Biotechnology, Faculty of Science, Chulalongkorn University..
National Center for Genetic Engineering and Biotechnology (BIOTEC); National Science and Technology Development Agency (NSTDA)..
Interdisciplinary Graduate Program on Maritime Administration, Graduate School, Chulalongkorn University..
Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Organismal Biology, Comparative Physiology.
2017 (English)In: Developmental and Comparative Immunology, ISSN 0145-305X, E-ISSN 1879-0089, Vol. 76, 229-237 p.Article in journal (Refereed) Published
Abstract [en]

A shrimp disease, the so-called acute hepatopancreatic necrosis disease (AHPND) is caused by a specific strain of Vibrio parahaemolyticus (VP) and it has resulted in significant losses to the global shrimp farming industry. In our previous study, three of tachylectin-like genes were cloned and characterized from the intestine of Penaeus monodon, designated as Penlectin5-1 (PL5-1), Penlectin5-2 (PL5-2) and Penlectin5-3 (PL5-3). These three genes all contain fibrinogen-related domain (FReD). The expression level of PL5-1, PL5-2 and PL5-3 was elevated in the stomach after oral administration with AHPND-causing V. parahaemolyticus 3HP (VP3HP). A polyclonal antibody to PL5-2 was successfully produced in a rabbit using the purified recombinant P15-2 as an immunogen, and this because only the predominant protein PL5-2 could be successfully purified from shrimp plasma by affinity chromatography using a N-Acetyl-oglucosamine column allowed us to perform functional studies of this lectin. The native purified PL5-2 protein had binding and agglutination activities towards VP3HR To further understand the functions and the involvements of this lectin in response to AHPND in shrimp, RNAi-mediated knockdown of PL5-1, PL5-2 or PL5-3 was performed prior to an oral administration of VP3HP. As a result, Penlectin5-silencing in shrimp challenged with VP3HP showed higher mortality and resulted in more severe histopathological changes in the hepatopancreas with typical signs of AHPND. These results therefore suggest a role for crustacean fibrinogen-related proteins (FRePs) in innate immune response during the development of AHPND, and maybe also during other infections.

Place, publisher, year, edition, pages
ELSEVIER SCI LTD , 2017. Vol. 76, 229-237 p.
Keyword [en]
Tachylectin, Lectin, EMS/AHPND, Innate immunity
National Category
Immunology Zoology
Identifiers
URN: urn:nbn:se:uu:diva-330526DOI: 10.1016/j.dci.2017.06.011ISI: 000407985100024PubMedID: 28655576OAI: oai:DiVA.org:uu-330526DiVA: diva2:1147959
Available from: 2017-10-09 Created: 2017-10-09 Last updated: 2017-10-09

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