Aeromonas veronii is an important pathogen causing freshwater fish sepsis and ulcer syndrome. An increasing number of cases have demonstrated its significance as an aquatic zoonotic agent. The purpose of this study was to ensure the safety of freshwater products by evaluating the infection status of edible freshwater fish. In this experiment, we isolated A. veronii from several species of apparently healthy freshwater fish, including Carassius auratus, Cyprinus carpio, Ctenopharyngodon idella, and Silurus asotus. A. veronii was identified through bacterial staining, culture characteristics, and 16S rDNA gene sequence. In addition, polymerase chain reaction (PCR) was used to investigate the distribution of seven major virulence genes, including aerolysin (aer: 88.51%), cytotoxic enterotoxin (act: 71.26%), serine proteinase (ser: 54.02%), adhesin (Aha: 40.23%), phospholipase (lip: 45.98%), nuclease (exu: 51.72%), and quorum sensing-controlled virulence factor (LuxS: 59.77%). In total, 496 strains of Aeromonas were isolated, including 87 strains of A. veronii. The isolates of A. veronii were Gram-negative, rod-shaped bacteria, and the colonies are yellow on Rimler-Shotts (RS) medium and showed greater than 99% homology with A. veronii ATCC35624 according to analyses of the 16S rDNA sequence. Nearly 50% of the A. veronii isolates carried at least four or more virulence genes, 25% of the isolates carried at least five types of virulence genes, and 59.77% isolates carried the LuxS gene, and the isolates carrying more virulence genes were found to be more virulent. These results are of great significance for further improving the food safety assessment of freshwater aquatic products.

Aeromonas veronii is one of the main pathogens causing freshwater fish sepsis and ulcer syndrome. More and more cases have shown that it has become an important zoonotic and aquatic agent. In this study, a A. veronii TH0426 mutant strain (ΔlamB) with an in‐frame deletion removed nucleotides 10–1,296 of the lamB gene was firstly constructed to investigate its functions. The results showed that the LD50 value of the mutant ΔlamB to zebrafish and mice was 13.7‐fold and 5.6‐fold higher than those of the wild‐type strain, respectively. The toxicity of wild‐type strain to EPC cells was 2.1‐fold and threefold higher than those of ∆lamB when infected for 1 and 2 hr. Furthermore, the ability of biofilm formation and the adhesion and invasion to EPC cells of ∆lamB significantly decreased for 5.6‐fold and 1.8‐fold separately. In addition, motility detection result indicated that ∆lamB lost the swimming ability. The results of flagellar staining and TEM demonstrated that the flagella of ∆lamB were shed. In general, the deletion of lamB gene caused a significant decrease in the virulence and adhesion of A. veronii TH0426, and it can be known that the lamB gene of A. veronii plays a crucial role in the pathogenesis.

Aeromonas veronii, a Gram-negative facultative anaerobic short bacillus bacterium, belongs to the family Aeromonadaceae and genus Aeromonas, and is an opportunistic pathogenic bacterium which infects humans, livestock and aquatic organisms (Rahman et al., 2002; Roberts et al., 2006). A. veronii is widely distributed in nature, especially in freshwater and estuary environments, and has strong environmental adaptability (Parte 2013). In recent years, the threat of A. veronii has become increasingly serious. While causing huge economic losses in the aquaculture industry, it also poses a threat to human health (Mencacci et al., 2003;

Eukaryotic cells can initiate several distinct self-destruction mechanisms to display essential roles for the homeostasis maintenance, development, and survival of an organism. Pyroptosis, a key response mode in innate immunity, also referred to as caspase-1-dependent proinflammatory programmed necrotic cell death activated by human caspase-1/4/5, or mouse caspase-1/11, plays indispensable roles in response to cytoplasmic insults and immune defense against infectious diseases. These inflammatory caspases are employed by the host to eliminate pathogen infections such as bacteria, viruses, protozoans, and fungi. Gasdermin D requires to be cleaved and activated by these inflammatory caspases to trigger the pyroptosis process. Physiological rupture of cells results in the release of proinflammatory cytokines, the alarmins IL-1β and IL-18, symbolizing the inflammatory potential of pyroptosis. Moreover, long noncoding RNAs play direct or indirect roles in the upstream of the pyroptosis trigger pathway. Here, we review in detail recently acquired insights into the central roles of inflammatory caspases, inflammasomes, and pyroptosis, as well as the crosstalk between pyroptosis and long noncoding RNAs in mediating infection immunity and pathogen clearance.

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