Aeromonas salmonicida is an ancient fish pathogen. Lysozymes are important molecules in the innate immune system that fight bacterial infections. The expression characteristics of C-type lysozyme in crucian carp infected with A. salmonicida and its antibacterial effect against A. salmonicida had not been investigated. Thus, we used bioinformatics to analyze the gene and protein characteristics of C-type lysozymes in crucian carp. Changes in C-type lysozyme expression before and after crucian carp infection with A. salmonicida were detected, and the in vitro antibacterial effect of recombinant carp C-type lysozyme on A. salmonicida was validated. The results showed that the coding DNA sequence region of the lysozyme gene sequence was 438 bp long, encoding 145 amino acids and containing two conserved catalytic sites: Glu53 and Asp69. Phylogenetic analysis revealed that crucian carp C-type lysozymes clustered with Cyprinus carpio lysozyme C. After crucian carp were infected with A. salmonicida, the gene and protein expression of C-type lysozymes in the liver, spleen, kidney, and hindgut were significantly upregulated, with the liver showing the highest upregulation that was 15 times higher than that in the uninfected group. In addition, recombinant C-type lysozyme exhibited significant antibacterial activity against A. salmonicida, with an average inhibition zone radius of 0.92 cm when using 40 μg recombinant lysozyme. In conclusion, this study reveals the important role of C-type lysozymes in the innate immune response of crucian carp and provides a theoretical basis for preventing crucian carp infection with A. salmonicida.

Aeromonas salmonicida is an age-old fish pathogen widely distributed in seawater and freshwater environments that causes significant economic losses to the global aquaculture industry. Genetic mutations and the emergence of thermophilic strains are factors in the continuous expansion of A. salmonicida’s host range. Beyond infecting fish, A. salmonicida poses a potential threat to mammalian and human health. This review synthesizes recent global research advances concerning A. salmonicida, encompassing strain characteristics, genomic features, virulence factors, and pathogenic mechanisms, as well as the clinical manifestations in infected fish and mammals, and discusses prevention and treatment methods. Particular emphasis is placed on evaluating the potential prophylactic roles of Chinese herbs and bacteriophages against A. salmonicida infection. Furthermore, the review provides perspectives on future research directions, diagnostics, and disease management, informed by contemporary domestic and international studies on this pathogen.

Yaks are an ideal model for investigating mammalian adaptation to high-altitude hypoxia; however, the underlying adaptive mechanisms remain unclear. Therefore, this study aimed to investigate the mechanisms underlying yak adaptation to high altitudes, focusing on the role of the PINK1/Parkin pathway. In particular, we established normoxic and hypoxic models of yak skeletal muscle satellite cells (SMSCs). In addition, we examined the relationship between PINK1/Parkin-mediated mitophagy and the activities of key enzymes involved in mitochondrial energy metabolism. At the tissue level, an increase in altitude significantly decreased p62 expression and upregulated LC3B-II expression. Notably, mitophagy levels and the expression of PINK1 and Parkin in the skeletal muscle, lungs, and myocardial tissues increased with altitude. At the cellular level, hypoxia markedly elevated the expression of PINK1 and Parkin proteins in SMSCs, induced the conversion of LC3-I to LC3-II, decreased p62 accumulation, significantly increased the number of autolysosomes, and enhanced autophagic flux. Hypoxia altered mitochondrial electron transport chain function, resulting in compensatory elevation of key enzyme activities in the mitochondrial respiratory chain. However, 3-methyladenine (3-MA) treatment reversed these hypoxia-induced changes. In conclusion, yak SMSCs sustain mitochondrial functional homeostasis under hypoxia via PINK1/Parkin-mediated mitophagy, effectively managing hypoxic stress.

Yaks (Bos grunniens) are a typical species inhabiting high-altitude environments; however, their molecular responses to hypoxic conditions remain incompletely understood. This study aimed to investigate associations among alanyl-transfer RNA synthetase 2 (AARS2) expression, lactylation of pyruvate dehydrogenase E1 alpha 1 (PDHA1) and carnitine palmitoyltransferase 2 (CPT2), and energy metabolism under hypoxic conditions in yaks. Oxygen-sensitive tissues (skeletal muscle, cardiac muscle, and lungs) collected from yaks at different altitudes, along with primary yak skeletal muscle cells, were analyzed using RT-qPCR, Western blotting, immunofluorescence (IF), and co-immunoprecipitation (co-IP). In tissues from the three altitude groups, AARS2 expression was higher in the higher-altitude groups (p < 0.05), whereas PDHA1 and CPT2 expression was lower (p < 0.01). Overall protein lactylation levels were also higher in tissues from the higher-altitude groups. Under hypoxic conditions, lactate levels and AARS2 expression increased in skeletal muscle cells, accompanied by increased activities of key glycolytic enzymes and decreased activities of enzymes related to mitochondrial oxidative phosphorylation. Galloflavin treatment reduced lactate levels and partially attenuated these metabolic changes. Endogenous co-IP detected lactylation of both PDHA1 and CPT2. Following siRNA-mediated knockdown of AARS2, the protein abundance of PDHA1 and CPT2 increased. Taken together, these findings support an association between hypoxia-induced lactate accumulation, increased AARS2 expression, PDHA1/CPT2 lactylation, and a shift in cellular energy metabolism toward glycolysis. This study provides a theoretical basis for further understanding hypoxia-related metabolic remodeling in yaks.