Dietary lutein mitigates high fat diet and lipopolysaccharide induced intestinal barrier dysfunction and immune inflammatory responses in juvenile black seabream (Acanthopagrus schlegelii).

High-fat diets (HFDs) can impair intestinal homeostasis and innate immune function in fish, whereas nutritional immunomodulation may provide an effective strategy to improve immune response to LPS challenge in aquaculture species. This study investigated whether dietary lutein (LU) alleviates HFD-induced immune dysfunction and improves the response of juvenile black seabream (Acanthopagrus schlegelii) to lipopolysaccharide (LPS) challenge. Fish were fed a normal-fat diet containing 8% lipid, an HFD containing 18% lipid, or the HFD supplemented with 0.125%, 0.25% and 0.50% LU for 10 weeks, followed by intraperitoneal injection with phosphate-buffered saline or LPS. Compared with the HFD group, dietary LU enhanced the levels of AKP, ACP, and ALB in serum and significantly decreased the levels of ALT and AST (P < 0.05). HFD altered intestinal morphology, as reflected by increased goblet cell number and reduced villus length, whereas LU supplementation up-regulated the expression of intestinal physical barrier related genes, including oclnα, cldn1 and cldn3, and suppressed the expression levels of mucosal immune stress genes, including grp78, ire1α and xbp1 and pro-inflammatory factors (nf-κb, tnfɑ) (P < 0.05). After LPS challenge, intestinal barrier-related genes were down-regulated, whereas LPS accumulation, complement activation, tlr/myd88/nf-κb signaling, inflammatory cytokine expression and apoptosis-related genes were markedly induced in the intestine and head kidney. Notably, LU supplementation modulated pparγ/rxr-related immune signaling, inhibited excessive TLR pathway activation, and attenuated LPS-induced inflammation and apoptosis. Overall, dietary LU alleviated HFD- and LPS-induced nonspecific immune impairment in juvenile black seabream, probably by maintaining intestinal barrier integrity and regulating the pparγ/rxr-tlr/nf-κb immune signaling pathway.