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Comparative transcriptome analysis reveals the different roles between hepatopancreas and intestine of Litopenaeus
Yilong Wang1, Baojie Wang2, Mei Liu2
1CAS Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, Qingdao 266071, China; Laboratory for Marine Biology and Biotechnology, Qingdao National Laboratory for Marine Science and Technology, Qingdao 266237, China; University of Chinese Academy of Sciences, Beijing 100049, China.
Abstract:
Aflatoxin B1 (AFB1) is a mycotoxin mainly produced by Aspergillus flavus and Aspergillus parasiticus contaminating food, feed ingredients and products of animal origin. In mammals, this toxin causes widespread organ-specific damage; it is immunotoxicity and could promote hepatotoxicity, alter intestinal functions and so on. In this study, we conducted transcriptome and histomorphology analyses of hepatopancreas and intestinal in Litopenaeus vannamei (L. vannamei) challenged with AFB1. Totally 12,014 and 1387 differentially expression genes (DEGs) were identified in the hepatopancreas and intestine, respectively. In hepatopancreas, a total of 1995 DEGs were mainly annotated and grouped into 18 processes or pathways related to animal immune system. With respect to intestine, a total of 152 DEGs were mainly annotated to 7 processes or pathways related to animal immune system. Meanwhile, we determined the relative mRNA expression of several crucial representative immune genes including Toll, immune deficiency (IMD), prophenoloxidase (proPO), Rab and glutathione S-transferase (GST) in the hepatopancreas and intestines of shrimp at 3-, 6-, 12-, 18-, 24- and 30-d after challenged by AFB1. Exposure to AFB1 increased mortality, decrease weight gain rate, severely destroyed the histomorphology of hepatopancreas and intestine, and resulted in the damaged of immune system of shrimp. The present data reveals the different roles between hepatopancreas and intestine of L. vannamei in immune response to AFB1 challenge, and provides insight into the molecular basis of the relationship between hepatopancreas and intestinal immunity during either homeostasis or inflammation.
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