The effects of chronic immune stimulation on muscle growth in rainbow trout.
Successful production of aquaculture species depends on efficient growth with low susceptibility to disease. Therefore, selection programs have focused on rapid growth combined with disease resistance. However, chronic immune stimulation diminishes muscle growth (a syndrome referred to as cachexia), and decreases growth efficiency in production animals, including rainbow trout. In mammals, recent results show that increased levels of pro-inflammatory cytokines, such as those seen during an immune assault, specifically target myosin and MyoD and inhibit muscle growth. This suggests that increased disease resistance in fish, a desired trait for production, may actually decrease the growth of muscle, the main aquacultural commodity. To test this possibility, a rainbow trout model of cachexia was developed and characterized. A six-week study was conducted in which rainbow trout were chronically immune stimulated by repeated injections of LPS. Growth indices were monitored, and whole body and muscle proximate analyses, real-time PCR, and Western blotting were conducted to examine the resulting cachectic phenotype. Muscle ratio was decreased in fish chronically immunostimulated, however expression levels of MyoD2 and myosin were not decreased compared to fish that were not immunostimulated, indicating that while muscle accretion was altered, the mechanism by which it occurred was somewhat different than that characterized in mammals. Microarray analysis was used to compare gene expression in fish that had been chronically immunostimulated versus those that had not to identify possible alternative mechanisms of cachexia in fish.
Johansen
Katherine A
KA
USDA-ARS, Hagerman Fish Culture Experiment Station, Hagerman, ID 83332, USA.
Sealey
Wendy M
WM
Overturf
Ken
K
D000818:Animals; D001835:Body Weight; D002100:Cachexia / Q000276:immunology / Q000378:metabolism / Q000662:veterinary; D005393:Fish Diseases / Q000276:immunology / Q000378:metabolism; D029941:Fish Proteins / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D018482:Muscle, Skeletal / Q000254:growth & development / Q000378:metabolism; D017570:MyoD Protein / Q000378:metabolism; D009218:Myosins / Q000378:metabolism; D020411:Oligonucleotide Array Sequence Analysis; D017686:Oncorhynchus mykiss / Q000254:growth & development* / Q000276:immunology* / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D029941:Fish Proteins; D008070:Lipopolysaccharides; C101548:MYOD2 protein, Oncorhynchus mykiss; D017570:MyoD Protein; D014409:Tumor Necrosis Factor-alpha; D009218:Myosins