Abstract
This study focuses on the relationship between myostatin (MyoS), myogenin (MyoG), and the growth hormone/insulin-like growth factor-1 (GH/IGF-1) axis for muscle growth and histopathological changes in muscle after an Aeromonas hydrophila infection. A total number of 90 Nile tilapia (55.85 g) were randomly allocated into two equal groups of three replicates each. The first group was an uninfected control group that was injected intraperitoneally (ip) with 0.2 ml phosphate buffer saline (PBS), while the second group was injected ip with 0.2 ml (1.3 × 10
CFU/ml) Aeromonas hydrophila culture suspension. Sections of white muscle and liver tissues were taken from each group 24 h, 48 h, 72 h, and 1 week after infection for molecular analysis and histopathological examination. The results revealed that with time progression, the severity of muscle lesions increased from edema between bundles and mononuclear inflammatory cell infiltration 24 h post-challenge to severe atrophy of muscle bundles with irregular and curved fibers with hyalinosis of the fibers 1 week postinfection. The molecular analysis showed that bacterial infection was able to induce the muscle expression levels of GH with reduced ILGF-1, MyoS, and MyoG at 24 h postinfection. However, time progression postinfection reversed these findings through elevated muscle expression levels of MyoS with regressed expression levels of muscle GH, ILGF-1, and MyoG. There have been no previous reports on the molecular expression analysis of the aforementioned genes and muscle histopathological changes in Nile tilapia following acute Aeromonas hydrophila infection. Our findings, collectively, revealed that the up-and down-regulation of the myostatin signaling is likely to be involved in the postinfection-induced muscle wasting through the negative regulation of genes involved in muscle growth, such as GH, ILGF-1, and myogenin, in response to acute Aeromonas hydrophila infection in Nile tilapia, Oreochromis niloticus.