Dataset Information

Vibrio alginolyticus influences quorum sensing-controlled phenotypes of acute hepatopancreatic necrosis disease-causing Vibrio parahaemolyticus.

ABSTRACT:

Background

Acute hepatopancreatic necrosis syndrome (AHPND) caused by Vibrio parahaemolyticus strain (VP_AHPND) impacts the shrimp industry worldwide. With the increasing problem of antibiotic abuse, studies on quorum sensing (QS) system and anti-QS compounds bring potential breakthroughs for disease prevention and treatment.

Methods

In this study, the cell-free culture supernatant (CFCS) and its extract of V. alginolyticus BC25 were investigated for anti-QS activity against a reporter bacteria, Chromobacterium violaceum DMST46846. The effects of CFCS and/ or extract on motility, biofilm formation and extracellular polymeric substances (EPSs) of VP_AHPND PSU5591 were evaluated. Moreover, the effects of V. alginolyticus BC25 on virulence of VP_AHPND PSU5591 were investigated by shrimp challenge test. The potentially active anti-QS compounds presented in the extract and effect on gene expression of VP_AHPND PSU5591 were identified.

Results

The CFCS of V. alginolyticus BC25 and its extract showed a significant anti-QS activity against the reporter bacteria as well as swimming and swarming motilities, biofilms, and EPSs production by VP_AHPND PSU5591. Transcriptome analysis revealed that V. alginolyticus BC25 extract significantly reduced the flagella genes involved in biofilm formation and iron-controlled virulence regulatory gene of VP_AHPND PSU5591. Whereas, the LuxR family transcriptional regulator gene, c-factor, a cell-cell signaling gene, and capsular polysaccharide were up-regulated. The potentially active anti-QS compounds identified in extract were Cyclo-(L-Leu-L-Pro), and Cyclo-(L-Phe-L-Pro). Furthermore, V. alginolyticus BC25 enhanced disease resistance against VP_AHPND PSU5591 in tested shrimp larvae.

Conclusion

These findings suggest that V. alginolyticus BC25 could provide natural anti-QS and anti-biofilms compounds and has great ability to be used as biocontrol agent against VP_AHPND infection in shrimp aquaculture.

SUBMITTER: Paopradit P

PROVIDER: S-EPMC8176930 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Acute hepatopancreatic necrosis disease (AHPND) is a newly emerging shrimp disease that has severely damaged the global shrimp industry. AHPND is caused by toxic strains of Vibrio parahaemolyticus that have acquired a "selfish plasmid" encoding the deadly binary toxins PirAvp/PirBvp To better understand the repertoire of virulence factors in AHPND-causing V. parahaemolyticus, we conducted a comparative analysis using the genome sequences of the clinical strain RIMD2210633 and of environmental non-AHPND and toxic AHPND isolates of V. parahaemolyticus Interestingly, we found that all of the AHPND strains, but none of the non-AHPND strains, harbor the antibacterial type VI secretion system 1 (T6SS1), which we previously identified and characterized in the clinical isolate RIMD2210633. This finding suggests that the acquisition of this T6SS might confer to AHPND-causing V. parahaemolyticus a fitness advantage over competing bacteria and facilitate shrimp infection. Additionally, we found highly dynamic effector loci in the T6SS1 of AHPND-causing strains, leading to diverse effector repertoires. Our discovery provides novel insights into AHPND-causing pathogens and reveals a potential target for disease control.IMPORTANCE Acute hepatopancreatic necrosis disease (AHPND) is a serious disease that has caused severe damage and significant financial losses to the global shrimp industry. To better understand and prevent this shrimp disease, it is essential to thoroughly characterize its causative agent, Vibrio parahaemolyticus Although the plasmid-encoded binary toxins PirAvp/PirBvp have been shown to be the primary cause of AHPND, it remains unknown whether other virulent factors are commonly present in V. parahaemolyticus and might play important roles during shrimp infection. Here, we analyzed the genome sequences of clinical, non-AHPND, and AHPND strains to characterize their repertoires of key virulence determinants. Our studies reveal that an antibacterial type VI secretion system is associated with the AHPND strains and differentiates them from non-AHPND strains, similar to what was seen with the PirA/PirB toxins. We propose that T6SS1 provides a selective advantage during shrimp infections.