Short-term feed deprivation alters immune status of surface mucosa in channel catfish (Ictalurus punctatus)

Abstract

Short-term feed deprivation (or fasting) is a common occurrence in aquacultured fish species whether due to season, production strategies, or disease. In channel catfish (Ictalurus punctatus) fasting impacts susceptibility to several bacterial pathogens including Flavobacterium columnare, the causative agent of columnaris disease. As columnaris gains entry through the gills and skin of fish, we examined here changes in transcriptional regulation induced in these surface mucosal tissues due to short-term (7 day) fasting. RNA-seq expression analysis revealed a total of 1,545 genes perturbed by fasting. Fasting significantly altered expression of critical innate immune factors in a manner consistent with lower immune fitness as well as dysregulating key genes involved in energy metabolism and cell cycling/proliferation. Downregulation of innate immune actors such as iNOS2b, Lysozyme C, and peptidoglycan recognition protein 6 is predicted to impact the delicate recognition/tolerance balance for commensal and pathogenic bacteria on the skin and gill. The highlighted expression profiles reveal potential mechanistic similarities between gut and surface mucosa and underscore the complex interrelationships between nutrition, mucosal integrity, and immunity in teleost fish.

Figure 1. Comparison of relative fold changes between RNA-seq and QPCR results in channel catfish.

Gene abbreviations are: Lysozyme g-like 1, LYGL1; Taxilin beta b, TXLNBB; Twinfilin-2, TWF2; Endothelial lipase precursor, LIPG; Stress-associated endoplasmic reticulum protein 2, SERP1; Anterior gradient protein 2 homolog precursor, AGR2; Phosphomannomutase 2, PMM2; Complement c4, C4; Nitric oxide synthase 2 b, inducible, iNOS2b; Vitelline membrane outer layer protein 1 homolog, VMO1.