Transcriptomic and microbiota response on Litopenaeus vannamei intestine subjected to acute sulfide exposure.

Abstract Harmful effects of water pollutants are myriad. Sulfide from water bodies affects the aquatic animals. Intestine barrier function serves as the front-line of animals defense. Our previous study confirmed the toxic effect of sulfide on intestine immune response of Litopenaeus vannamei , but the underlying mechanisms remained elusive. Therefore, in this study, we investigated the transcriptomic and microbiota responses of the L. vannamei intestine subjected to acute sulfide exposure. Sulfide decreased bacterial richness and altered the intestine microbiota composition. Specifically, sulfide increased the abundances of Bacteroidetes and Actinobacteria, but decreased the abundance of Proteobacteria. At the genus level, sulfide increased typical cellulolytic characteristics bacteria, such as Formosa , Sphingomonas , and Demequina. RNA-seq analysis identified differential expression of 1799 genes (701 up-regulated and 1098 down-regulated) were grouped into 267 pathways. The most enriched pathway 'amoebiasis' was related to the intestine mucus homeostasis. A number of immune-related genes associated with antimicrobial, antioxidant, pathogen attachment and recognition, and apoptosis processes in contrasting accessions; they were correlated with the abundance of intestine bacterial at the phylum level. This study provides an insight into the mechanisms associated with molecular and microbiota response and processes involved in adaptation strategies towards sulfide stress. Highlights • Transcriptomic and microbiome responses of the Litopenaeus vannamei intestine exposed to sulfide stress was studied. • Sulfide decreased bacterial richness and altered the intestine microbiota composition. • 701 up-regulated and 1098 down-regulated genes differentially expressed in response to sulfide exposure. • The most enriched pathway "amoebiasis" was related to the intestine mucus homeostasis. • We speculated a potential mechanism of intestine barrier function in the contrasting accessions towards sulfide exposure. [ABSTRACT FROM AUTHOR]