Feeding faba beans to grass carp could crisp its muscle texture to avoid softening, the relationship between texture formation throughout the crisping process and the critical lipids regulating the fish quality has not yet been clarified. Herein, an 60-day nutritional trial and untargeted lipidomic analysis was used to study the changes of lipids in crisp grass carp dorsal muscle. A total of 1036 lipids were remarkably different between ordinary and crisp grass carp. The concentrations of the LPC, LPE, PG, Cer, Hex2Cer, SM, MG and MGMG were positively correlated with hardness and springiness, and the CL, TG, PMe, WE, dMePE and AcCa were negative correlation. High content of lipids involved in storage in ordinary grass carp, such as glycerophospholipids, polyunsaturated and saturated fatty acid content. In contrast, high content of membrane components in crisp grass carp, such as monounsaturated fatty acid, sphingolipid and glycerolipids content, and the distribution of PUFA in lipid molecules was related to lipid biosynthesis. This study might provide some insights into improved knowledge of the association between meat texture and lipid molecules in fish fed with faba bean.

Growth stage is a key factor influencing the composition and richness of the porcine gut microbiota. The stage-specific alterations in gut microbiota of indigenous Chinese pig breeds and cultivated breeds remain to be elucidated. This study conducted 16S rRNA sequencing analysis on fecal microbiota from Dahe black pigs across distinct growth stages. Samples included lactating sows, suckling piglets, weaned piglets, pigs weighing 50–100 kg, pigs weighing 120–150 kg, and pigs weighing > 200 kg. The results indicated that Escherichia shigella (12.4% vs. 16.2%), Lactobacillus (5.9% vs. 6.3%), and Rikenellaceae RC9 gut group (3.9% vs. 4.2%) were dominant genera shared between lactating sows and suckling piglets. The relative abundance of Eubacterium brachy group was significantly higher in lactating sows, whereas Flavonifractor was significantly lower compared to suckling piglets (p < 0.05). Compared to pigs weighing > 120 kg, lactating sows exhibited 22 differentially abundant genera, including Escherichia shigella, Cloacibacillus, Fusobacterium, Faecalibacterium, and Prevotella (p < 0.05). In suckling piglets, Firmicutes and Bacteroidota constituted 47.4% and 27.3% of the microbiota, respectively. Their relative abundance increased with body weight, reaching 52.6% and 33.3% in pigs weighing > 200 kg. Proteobacteria decreased from 17.3% in suckling piglets to 2.0% in >200 kg pigs. Spirochaetota declined from 2.5% in suckling piglets to 0.9% in weaned piglets and then increased to 6.9% in >200 kg pigs. Lactobacillus peaked at 15.7% in weaned piglets, while Escherichia shigella reached its maximum (16.2%) in suckling piglets, both gradually declining thereafter. Streptococcus abundance remained relatively stable (1.1% in suckling piglets; 4.5% in weaned piglets). Prevotellaceae NK3B31 group registered 2.9% in suckling piglets, increased to 7.1% in weaned piglets, and then declined to 2.6% in >200 kg pigs. Mitsuokella, Bilophila, Succinivibrio, Romboutsia, and Desulfovibrio were identified as the top five genera discriminating suckling and weaned piglets. Similarly, Lachnospiraceae XPB1014 group, Clostridium sensu stricto 1, Turicibacter, Quinella, and p 1088 a5 gut group were key discriminators between weaned piglets and 50–100 kg pigs. These identified microbial taxa represent potential candidate targets for modulating the developmental timing of growth phases in pigs, offering possibilities for either advancing or delaying specific physiological timepoints.

The intestinal immune barrier is a developed and complex immune system, and there is a fine synergy between it and the induced immune response. Short-chain fatty acids (SCFAs) are the main metabolites of intestinal microbial fermentation. In the cecum of pigs, SCFAs not only provide energy for the host but also participate in regulating the function of the intestinal immune system. The purpose of this study was to explore the mechanism of SCFAs in the regulation of immune gene expression in porcine cecum. SCFAs content and mRNA expression levels of immune genes in cecum were detected, and Gene Ontology (GO) function annotation, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, Protein-Protein Interaction Networks (PPI) network construction, key gene identification, and correlation analysis were performed. The results showed that the content of SCFAs in the cecum of Dahe black pigs (DHB) was lower than that of Dahe pigs (DH). There were significant differences in mRNA expression of some immune genes between the two groups. GO functional annotation found terms related to cytokine activity and protein heterodimerization activity; the KEGG pathway was enriched in several pathways related to intestinal immunity. The PPI network identified Interleukin-6 (IL-6), Interleukin-8 (IL-8), Interleukin-10 (IL-10), Interleukin-17A (IL-17A), and Interleukin-18 (IL-18) as key proteins. The correlation analysis showed that acetic acid and valerate were closely related to the immune response. In this study, the differences in cecal short-chain fatty acids and the immune barrier between Dahe pigs and Dahe black pigs were compared, which provided a theoretical basis for improving the intestinal immunity of pigs.

The beta T-cell receptor (TRB) expressed by beta T cells is essential for foreign antigen recognition. The TRB locus contains a TRBV family that encodes three complementarity determining regions (CDRs). CDR1 is associated with antigen recognition and interactions with MHC molecules. In contrast to domestic pigs, African suids lack a 284-bp segment spanning exons 1 and 2 of the TRBV27 gene that contains a sequence encoding CDR1. In this study, we used the African swine fever virus (ASFV) as an example to investigate the effect of deleting the TRBV27-encoded CDR1 on the resistance of domestic pigs to exotic pathogens. We first successfully generated TRBV27-edited fibroblasts with disruption of the CDR1 sequence using CRISPR/Cas9 technology and used them as donor cells to generate gene-edited pigs via somatic cell nuclear transfer. The TRBV-edited and wild-type pigs were selected for synchronous ASFV infection. White blood cells were significantly reduced in the genetically modified pigs before ASFV infection. The genetically modified and wild-type pigs were susceptible to ASFV and exhibited typical fevers (>40 °C). However, the TRBV27-edited pigs had a higher viral load than the wild-type pigs. Consistent with this, the gene-edited pigs showed more clinical signs than the wild-type pigs. In addition, both groups of pigs died within 10 days and showed similar severe lesions in organs and tissues. Future studies using lower virulence ASFV isolates are needed to determine the relationship between the TRBV27 gene and ASFV infection in pigs over a relatively long period.

Background: While Toxoplasma gondii infection poses a significant health threat, its impact on the localized intestinal lipid metabolism remains unclear. Methods: Thus, this study established an acute infection model in BALB/cJ mice and analyzed the colonic contents collected 10 days post-infection via untargeted lipidomics. The lipid profiles of the two groups diverged substantially, with a clear separation evident between infection and control conditions. Results: We identified 65 upregulated and 87 downregulated differential lipids, primarily falling into the glycerophospholipids and sphingolipids categories. Pathway enrichment analysis revealed that the choline metabolism in cancer and glycerophospholipid metabolism pathways was pinpointed as being among the most perturbed following infection. Correlation and network analyses further suggested that key molecules, such as LPC (20:4) and LPA (18:0), may mediate these metabolic pathway abnormalities by regulating related enzymatic activities. Conclusions: This systematic characterization of the intestinal lipid metabolic landscape in mice during acute T. gondii infection revealed the host intestinal lipid metabolic reprogramming induced by T. gondii infection. The findings offer a novel metabolic perspective for understanding T. gondii pathogenesis and host–parasite interactions.