Temporal Influence of Transport Length on Epidermal Barrier Integrity, Mucin Transcription, and Goblet Cell Kinetics in Red Tilapia (Oreochromis sp.) Fry

Red tilapia (Oreochromis sp.) fry are routinely transported between hatcheries and grow out farms, yet the effects of transport duration on epidermal barrier-associated responses and goblet cells remain poorly defined. This study assessed the impact of simulated transport on epidermal morphology, immune-related gene expression and goblet cell density in red tilapia fry. Fish were assigned to four groups (0, 5, 12 and 20 h of transport). Skin samples were analyzed for relative mRNA expression of 10 genes associated with tight junction proteins, mucins, antimicrobial peptides and cytokines using RT-qPCR, and for epidermal goblet cell density by histology. Transport significantly modulated eight genes, forming three co-expression clusters associated with inflammatory, barrier-related, and mucus-related responses, with mainly non-linear time courses. MUC2, DB-4, IL-1β, and TGF-β1b showed transient increases at 5–12 h, whereas MUC5AC and claudin transcripts increased earlier and approached control levels at 20 h. Goblet cell density remained relatively stable up to 12 h but declined after 20 h, coinciding with changes in MUC2 and MUC5AC expression and suggesting altered mucosal responses during prolonged transport. Overall, transport durations ≤ 12 h were associated with relatively stable epidermal responses, whereas 20 h induced pronounced changes in goblet cell density and barrier-associated gene expression. These findings provide information that may assist future optimization of transport practices in tilapia aquaculture. Transport stress in red tilapia fry induces rapid defensive responses, significantly modulating gene expression and mucosal dynamics; this is characterized by increased mucus production, goblet cell density, and early upregulation of mucins (MUC2), followed by later increases in tight junction genes and anti-inflammatory cytokines, alongside a temporary downregulation of antimicrobial peptides.