Comparative analysis of midgut bacterial community under Vibrio splendidus infection in Apostichopus japonicus with hindgut as a reference

Abstract

Animal gut harbors diverse microbes in the protection against pathogen invasion and the regulation of host immune responses. In our previous work, we found that environmental factors destroy hindgut intestinal flora to promote pathogen infection in sea cucumber. Midgut microbiota could protect host from pathogen infection via producing of antibiotics and enzymes in human and insect. To address the function role of midgut microbiota, the bacterial community in the midgut of Apostichopus japonicus was assessed using 16S rRNA sequencing technology, as well as following the Vibrio splendidus infection in this study. Results showed that the relative abundance of Actinobacteria in the midgut under V. splendidus infection was lower compared to the normal midgut, and the Clostridiaceae, Ruminococcaceae and Lachnospiraceae were increased under pathogen infection in the midgut at the family level. Notably, the abundance of V. splendidus was significantly lower in the midgut than hindgut in both healthy and diseased conditions. Function analysis indicated that the basal metabolic pathways were significantly higher in midgut than hindgut under diseased condition, while, the signaling molecules and interaction, xenobiotics biodegradation and metabolism pathways with the bacteria were lower in midgut than hindgut under V. splendidus infection. Less cooperative interactions were dominant in the hindgut in response to pathogen infection, but more cooperative and complex interactions predominated in the microbial community in the midgut under diseased condition. Among them, the interaction with Vibrionaceae was significantly decreased in the midgut compared with the hindgut under V. splendidus infection. All our results suggested the difference function role of the microbiota in midgut and hindgut of sea cucumber, in which V. splendidus was more likely to colonized in the hindgut and promote the occurrence and development of skin ulceration syndrome, rather than the midgut.