Host defense peptides (HDPs) play a critical role in innate immunity. Specific modulation of endogenous HDP synthesis by dietary compounds has been regarded as a novel approach to boost immunity and disease resistance in animal production. 1,25-dihydroxy vitamin D₃ (1,25D₃) is well known as a powerful HDP inducer in humans, but limited information about the effect of 1,25D₃ on HDPs in poultry is available. Here, we sought to examine whether 1,25D₃ could stimulate avian β-defensin (AvBD) expression in chickens. We used chicken embryo intestinal epithelial cells (CEIEPCs) and peripheral blood mononuclear cells (PBMCs) to study the effect of 1,25D₃ on the expression of AvBDs. We observed that 1,25D₃ is able to up-regulate the expression of several AvBDs in CEIEPCs and PBMCs, whereas it increased the amounts of AvBD4 mRNA in CEIEPCs only in the presence of lipopolysaccharide (LPS). On the other hand, LPS treatment not only inhibited the expression of CYP24A1 but also altered the expression pattern of VDR in CEIEPCs. Furthermore, AvBDs were not directly regulated by 1,25D₃, as cycloheximide completely blocked 1,25D₃-induced expression of AvBDs. Our observations suggest that 1,25D₃ is capable of inducing AvBD gene expression and is a potential antibiotic alternative through augmentation of host innate immunity as well as disease control in chickens.

Host gut microbiomes play an important role in animal health and resilience to conditions, such as malnutrition and starvation. These host-microbiome relationships are poorly understood in the marine mussel Perna canaliculus, which experiences significant variations in food quantity and quality in coastal areas. Prolonged starvation may be a contributory factor towards incidences of mass mortalities in farmed mussel populations, resulting in highly variable production costs and unreliable market supplies. Here, we examine the gut microbiota of P. canaliculus in response to starvation and subsequent re-feeding using high-throughput amplicon sequencing of the 16S rRNA gene. Mussels showed no change in bacterial species richness when subjected to a 14-day starvation, followed by re-feeding/recovery. However, beta bacteria diversity revealed significant shifts (PERMANOVA p-value < 0.001) in community structure in the starvation group and no differences in the subsequent recovery group (compared to the control group) once they were re-fed, highlighting their recovery capability and resilience. Phylum-level community profiles revealed an elevation in dominance of Proteobacteria (ANCOM-BC p-value <0.001) and Bacteroidota (ANCOM-BC p-value = 0.04) and lower relative abundance of Cyanobacteria (ANCOM-BC p-value = 0.01) in the starvation group compared to control and recovery groups. The most abundant genus-level shifts revealed relative increases of the heterotroph Halioglobus (p-value < 0.05) and lowered abundances of the autotroph Synechococcus CC9902 in the starvation group. Furthermore, a SparCC correlation network identified co-occurrence of a cluster of genera with elevated relative abundance in the starved mussels that were positively correlated with Synechococcus CC9902. The findings from this work provide the first insights into the effect of starvation on the resilience capacity of Perna canaliculus gut microbiota, which is of central importance to understanding the effect of food variation and limitation in farmed mussels.

This study aimed to investigate the effects of oxidized fish oil (OFO) on growth performance, intestinal health, and antioxidant function and to determine the minimum concentration of oxidized fish oil to cause irreversible damage to the intestinal tissue structure of zebrafish. A 30-day feeding trial on zebrafish (average weight 0.054 g) was conducted in triplicate groups of fish fed four test diets containing different concentrations of OFO: 0% OFO (OFF, blank control), 2% OFO (OF1), 4% OFO (OF2), and 6% OFO (OF3). The body weight gain (WG), specific growth rates (SGR), feed conversion ratio (FCR), survival rate (SR), and antioxidant function {glutathione peroxidase (GSH-PX), total superoxide dismutase (T-SOD), catalase (CAT), and malondialdehyde (MDA)} were recorded. The intestinal structure was observed at the end of the trial. After the 14-day experimental period, Final body weight (FBW), WG, and SGR decreased significantly with the increase in the concentration of feed OFO (P < 0.05), while FCR showed a downward trend. The activity of T-SOD decreased significantly, the activities of GSH-PX and CAT, and the MDA content increased significantly with the increase in the concentration of feed OFO (P < 0.05). The intestinal morphological damage score showed an upward trend with the increase in the concentration of OFO, and it was significantly higher in group OF2 and OF3 than in group OF1 (P < 0.05). After the 28-day test period, the experimental indexes and intestinal antioxidant function trends were the same as those on 14 days. The increased OFO concentration significantly increased the intestinal morphological injury score (P < 0.05). These results demonstrated that adding 4% OFO to the feed for 14 days could induce irreversible damage to the intestinal tissue structure, weaken the antioxidant function, and decrease the growth performance of zebrafish.