Metabolic Alterations in Shrimp Stomach During Acute Hepatopancreatic Necrosis Disease and Effects of Taurocholate on Vibrio parahaemolyticus.

Ramya Kumar,Shih-Shun Lin,Yi-Min Chen,Han-Ching Wang,Teng-Chun Tung,Tze Hann Ng,Yi-Lun Chen,Che-Chih Chang

doi:10.3389/fmicb.2021.631468

Abstract

Acute hepatopancreatic necrosis disease (AHPND), a recently emerged bacterial shrimp disease, has increased shrimp mortality and caused huge economic losses in many Asian countries. However, molecular factors underlying pathogenesis of this disease remain largely unknown. Our objective was to characterize metabolic alterations in shrimp stomach during AHPND and determine effects of taurocholate on AHPND-causing Vibrio parahaemolyticus. Based on metabolomics, pathways for lipid metabolism and for primary bile acid (BA) synthesis were majorly affected following AHPND infection. Bile acid metabolites, namely taurocholate, were downregulated in the metabolomics database. This prompted us to study effects of taurocholate on biofilm formation, PirABvp toxin release and biofilm detachment capabilities in AHPND-causing V. parahaemolyticus. Treatment of this bacterium with high concentration of taurocholate, a primary bile acid, induced biofilm formation, PirABvp toxin release and facilitated the dispersion of bacterial cells. Taken together, our findings suggest that AHPND infection can affect the lipid metabolites in shrimp stomach, and further suggest that the primary bile acid taurocholate is important for the virulence of AHPND-causing V. parahaemolyticus.

Highlights

In recent decades, growing demands for shrimp have transformed the industry from traditional farming into widespread commercial production (Walker and Mohan, 2009)
In principal component analysis (PCA) analysis (Figure 1B), distinct clusters formed by the metabolites of 5HP-infected shrimp samples in both POS and NEG ion modes implied that composition of the metabolites in the 5HP-infected group was different from that of the S02 and Tryptic soy broth (TSB) controls
Since the bile acid metabolites were altered during Acute hepatopancreatic necrosis disease (AHPND) infection (Figure 3A), we examined the expression of the bile acid synthesis genes in stomach samples taken from the same S02-challenged and 5HP-infected shrimp at 12 and 24 hpi

Summary

Introduction

In recent decades, growing demands for shrimp have transformed the industry from traditional farming into widespread commercial production (Walker and Mohan, 2009). Since 2009, many Southeast Asian countries have been affected by outbreaks of acute hepatopancreatic necrosis disease (AHPND), a bacterial disease caused by virulent strains of Vibrio parahaemolyticus (Tran et al, 2013; Shinn et al, 2018; Kumar et al, 2020b). The AHPND-causing V. parahaemolyticus is a virulent pathogen that affects. It has already been shown that AHPND-causing bacteria initially colonize the shrimp stomach; the binary PirAvp and PirBvp toxins produced by these pathogenic bacteria are released from stomach into the hepatopancreas, causing necrosis of the epithelial cells and infiltration of hemocytes into the hepatopancreas (Lai et al, 2015; Ng et al, 2018; Kumar et al, 2020a)

Objectives

Methods

Results

Discussion

Conclusion