Dataset Information

Transcriptomic analysis of Pacific white shrimp (Litopenaeus vannamei, Boone 1931) in response to acute hepatopancreatic necrosis disease caused by Vibrio parahaemolyticus.

ABSTRACT: Acute hepatopancreatic necrosis disease (AHPND), caused by marine bacteria Vibrio Parahaemolyticus, is a huge problem in shrimp farms. The V. parahaemolyticus infecting material is contained in a plasmid which encodes for the lethal toxins PirABVp, whose primary target tissue is the hepatopancreas, causing sloughing of epithelial cells, necrosis, and massive hemocyte infiltration. To get a better understanding of the hepatopancreas response during AHPND, juvenile shrimp Litopenaeus vannamei were infected by immersion with V. parahaemolyticus. We performed transcriptomic mRNA sequencing of infected shrimp hepatopancreas, at 24 hours post-infection, to identify novel differentially expressed genes a total of 174,098 transcripts were examined of which 915 transcripts were found differentially expressed after comparative transcriptomic analysis: 442 up-regulated and 473 down-regulated transcripts. Gene Ontology term enrichment analysis for up-regulated transcripts includes metabolic process, regulation of programmed cell death, carbohydrate metabolic process, and biological adhesion, whereas for down-regulated transcripts include, microtubule-based process, cell activation, and chitin metabolic process. The analysis of protein- protein network between up and down-regulated genes indicates that the first gene interactions are connected to oxidation-processes and sarcomere organization. Additionally, protein-protein networks analysis identified 20-top highly connected hub nodes. Based on their immunological or metabolic function, ten candidate transcripts were selected to measure their mRNA relative expression levels in AHPND infected shrimp hepatopancreas by RT-qPCR. Our results indicate a close connection between the immune and metabolism systems during AHPND infection. Our RNA-Seq and RT-qPCR data provide the possible immunological and physiological scenario as well as the molecular pathways that take place in the shrimp hepatopancreas in response to an infectious disease.

SUBMITTER: Velazquez-Lizarraga AE

PROVIDER: S-EPMC6692014 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Transcriptomic analysis of Pacific white shrimp (Litopenaeus vannamei, Boone 1931) in response to acute hepatopancreatic necrosis disease caused by Vibrio parahaemolyticus.

Velázquez-Lizárraga Adrián E AE Juárez-Morales José Luis JL Racotta Ilie S IS Villarreal-Colmenares Humberto H Valdes-Lopez Oswaldo O Luna-González Antonio A Rodríguez-Jaramillo Carmen C Estrada Norma N Ascencio Felipe F

PloS one 20190813 8

Acute hepatopancreatic necrosis disease (AHPND), caused by marine bacteria Vibrio Parahaemolyticus, is a huge problem in shrimp farms. The V. parahaemolyticus infecting material is contained in a plasmid which encodes for the lethal toxins PirABVp, whose primary target tissue is the hepatopancreas, causing sloughing of epithelial cells, necrosis, and massive hemocyte infiltration. To get a better understanding of the hepatopancreas response during AHPND, juvenile shrimp Litopenaeus vannamei were ...[more]

PMID: 31408485

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Project description:Acute hepatopancreatic necrosis disease (AHPND) has caused a huge economic loss to shrimp aquaculture. Vibrio parahaemolyticus (VpAHPND) is regarded as a major causative agent of AHPND in the Pacific white shrimp Litopenaeus vannamei. However, knowledge about how shrimp resist to AHPND is very limited. In order to learn the molecular mechanisms underlying AHPND resistance of shrimp, comparison between disease-resistant family and susceptible family of L. vannamei were performed at transcriptional and metabolic levels. Integrated analysis of transcriptomics and metabolomics on hepatopancreas of shrimp, the target tissue of VpAHPND, showed that significant differences existed between resistant family and susceptible family of shrimp. The susceptible family showed higher level of glycolysis, serine-glycine metabolism, purine and pyrimidine metabolism, but lower level of betaine-homocysteine metabolism in the hepatopancreas in comparison with the resistant family without VpAHPND infection. Curiously, VpAHPND infection induced up-regulation of glycolysis, serine-glycine metabolism, purine metabolism, pyrimidine metabolism, and pentose phosphate pathway, and down-regulation of betaine-homocysteine metabolism in resistant family. In addition, arachidonic acid metabolism and some immune pathways, like NF-κB and cAMP pathways, were up-regulated in the resistant family after VpAHPND infection. In contrast, amino acid catabolism boosted via PEPCK-mediated TCA cycle flux was activated in the susceptible family after VpAHPND infection. These differences in transcriptome and metabolome between resistant family and susceptible family might contribute to the resistance of shrimp to bacteria. IMPORTANCE Vibrio parahaemolyticus (VpAHPND) is a major aquatic pathogen causing acute hepatopancreatic necrosis disease (AHPND) and leads to a huge economic loss to shrimp aquaculture. Despite the recent development of controlling culture environment, disease resistant broodstock breeding is still a sustainable approach for aquatic disease control. Metabolic changes occurred during VpAHPND infection, but knowledge about the metabolism in resistance to AHPND is very limited. Integrated analysis of transcriptome and metabolome revealed the basal metabolic differences exhibited between disease-resistant and susceptible shrimp. Amino acid catabolism might contribute to the pathogenesis of VpAHPND and arachidonic acid metabolism might be responsible for the resistance phenotype. This study will help to enlighten the metabolic and molecular mechanisms underlying shrimp resistance to AHPND. Also, the key genes and metabolites of amino acid and arachidonic acid pathway identified in this study will be applied for disease resistance improvement in the shrimp culture industry.

Project description:Acute hepatopancreatic necrosis disease (AHPND), a high-mortality-rate shrimp disease, is caused by specific Vibrio parahaemolyticus (Vp) strains with a plasmid encoding the PirABVp toxins. As a bacterial pathogen, the invasion of AHPND-causing Vp might impose pressure on commensal microbiota in the shrimp gut, while the relationship between the pathogenesis of AHPND and the dysbiosis of gut bacterial communities remains unclear. Here we explored the temporal changes of shrimp gut microbiota in response to AHPND-causing and non-AHPND-causing Vp strains, with the non-infected controls as a baseline of the shrimp gut microbiota. The diversity and composition of bacterial communities from 168 gut samples (covering three treatments at seven time points with eight individuals per set) were investigated using 16S rRNA gene metabarcoding with high-throughput sequencing. The results showed that (i) species diversity of gut bacterial communities declined in Vp-infected shrimp, independent of the strain pathogenicity; (ii) taxonomic compositions of gut bacterial communities were significantly different between shrimp infected by AHPND-causing and non-AHPND-causing Vp strains; (iii) short-term (within 6 hours) compositional shifts in the gut microbiota were found only in AHPND-causing Vp-infected shrimp; (iv) the gut microbiota of AHPND-causing Vp-infected shrimp was enriched with genera Photobacterium and Vibrio, with a decline in Candidatus Bacilliplasma; and (v) functional predictions suggested the loss of normal metabolism due to compositional shifts in the gut microbiota. Our work reveals distinct features of community dynamics in shrimp gut microbiota, associated with pathogenic versus non-pathogenic Vibrio infections, providing a new perspective of the pathogenesis of AHPND. IMPORTANCE Shrimp production is continually threatened by newly emerging diseases, such as AHPND, which is caused by specific Vp strains. Previous studies on the pathogenesis of AHPND have mainly focused on the histopathology and immune responses of the host. However, more attention needs to be paid to the gut microbiota, which acts as the first barrier to pathogen colonization. In this study, we revealed that shrimp gut microbiota responded differently to pathogenic and non-pathogenic Vp strains, with bacterial genera Photobacterium and Vibrio enriched in pathogenic Vp-infected shrimp, and Candidatus Bacilliplasma enriched in non-pathogenic Vp-infected shrimp. Moreover, functional predictions suggested that changes in taxonomic compositions would further affect normal metabolic functions, emphasizing the importance of sustaining an equilibrium in the gut microbiota. Several biomarkers associated with specific microbial taxa and functional pathways were identified in our data sets, which help predict the incidence of disease outcomes.

Project description:Harmful algae blooms (HABs) are a conspicuous phenomenon that affect the coastal zone worldwide. Aquaculture industry zones are not excluded from being affected by HAB that cause organism mortality and jeopardize their innocuity due to the contamination by phytotoxins with the concomitant economic losses. Direct ingestion of metabolites from HAB species or organisms contaminated with phycotoxins together with dermal absorption of dissolved metabolites (DM), including toxins, are the two main routes of poisoning. From these poisoning routes, the effect of DM, particularly paralytic shellfish toxins (PST), has been relatively understudied. This intoxication route can be conspicuous and could be involved in many significant mortalities of cultivated marine organisms. In this study, white shrimp juveniles (2.1 g wet weight) of Litopenaeus vannamei were exposed to extracts of 104, 105 and 106 cells/L of the dinoflagellate Gymnodinium catenatum, a PST producer. The experiment ended after 17 h of exposure when shrimps exposed to 106 cells/L extract started to die and the rest of the shrimps, from this and other treatments, did not respond to gentle physical stimulus and their swimming activity was low and erratic. Toxin concentrations were determined using high performance liquid chromatography while qualitative and quantitative histological damages were assessed on the tissues. In general, most toxins were accumulated in the hepatopancreas where more than 90% were found. Other tissues such as intestine, muscle, and gills contained less than 10% of toxins. Compared to the control, the main significative tissue damages were, loss of up to 80% of the nerve cord, 40% of the muscle coverage area, and reduction of the gill lamella width. Also, atrophy in hepatopancreas was observed, manifested by a decrease in the height of B cells, lumen degeneration and thinning of tubules. Some damages were more evident when shrimps were exposed to higher concentrated extracts of G. catenatum, however, not all damages were progressive and proportional to the extract concentration. These data confirm that PST dissolved enter the shrimp, possibly via the gills, and suggest that dissolved metabolites, including PST, may cause tissue damage. Other dissolved metabolites produced by G. catenatum, alone or in synergy, may also be involved. These results also pointed out the importance of dissolved molecules produced for this dinoflagellate and the potential effect on cultured shrimp.

Dataset Information

Transcriptomic analysis of Pacific white shrimp (Litopenaeus vannamei, Boone 1931) in response to acute hepatopancreatic necrosis disease caused by Vibrio parahaemolyticus.

Publications

Transcriptomic analysis of Pacific white shrimp (Litopenaeus vannamei, Boone 1931) in response to acute hepatopancreatic necrosis disease caused by Vibrio parahaemolyticus.

Similar Datasets

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