Increased Ingestion of Hydroxy-Methionine by Both Sows and Piglets Improves the Ability of the Progeny to Counteract LPS-Induced Hepatic and Splenic Injury with Potential Regulation of TLR4 and NOD Signaling.

Methionine, as an essential amino acid, play roles in antioxidant defense and the regulation of immune responses. This study was designed to determine the effects and mechanisms of increased consumption of methionine by sows and piglets on the capacity of the progeny to counteract lipopolysaccharide (LPS) challenge-induced injury in the liver and spleen of piglets. Primiparous sows (n = 10/diet) and their progeny were fed a diet that was adequate in sulfur amino acids (CON) or CON + 25% total sulfur amino acids as methionine from gestation day 85 to postnatal day 35. A total of ten male piglets were selected from each treatment and divided into 2 groups (n = 5/treatment) for a 2 × 2 factorial design [diets (CON, Methionine) and challenge (saline or LPS)] at 35 d old. After 24 h challenge, the piglets were euthanized to collect the liver and spleen for the histopathology, redox status, and gene expression analysis. The histopathological results showed that LPS challenge induced liver and spleen injury, while dietary methionine supplementation alleviated these damages that were induced by the LPS challenge. Furthermore, the LPS challenge also decreased the activities of GPX, SOD, and CAT and upregulated the mRNA and(or) protein expression of TLR4, MyD88, TRAF6, NOD1, NOD2, NF-kB, TNF-α, IL-8, p53, BCL2, and COX2 in the liver and (or) spleen. The alterations of GPX and SOD activities and the former nine genes were prevented or alleviated by the methionine supplementation. In conclusion, the maternal and neonatal dietary supplementation of methionine improved the ability of piglets to resist LPS challenge-induced liver and spleen injury, potentially through the increased antioxidant capacity and inhibition of TLR4 and NOD signaling pathway.

Increased Consumption of Sulfur Amino Acids by Both Sows and Piglets Enhances the Ability of the Progeny to Adverse Effects Induced by Lipopolysaccharide.

This study determined the effects of increased consumption of sulfur amino acids (SAA), as either DL-Met or Hydroxy-Met (OH-Met), by sows and piglets on their performance and the ability of the progeny to resist a lipopolysaccharide (LPS) challenge. Thirty primiparous sows were fed a diet adequate in SAA (CON) or CON + 25% SAA, either as DL-Met or OH-Met from gestation day 85 to postnatal day 21. At 35 d old, 20 male piglets from each treatment were selected and divided into 2 groups (n = 10/treatment) for a 3 × 2 factorial design [diets (CON, DL-Met or OH-Met) and challenge (saline or LPS)]. OH-Met and/or DL-Met supplementation increased (p ≤ 0.05) piglets' body weight gain during day 0-7 and day 7-14. Sow's milk quality was improved in the supplemented treatments compared to the CON. The LPS challenge decreased (p ≤ 0.05) piglets' performance from 35 to 63 d and increased (p ≤ 0.05) the levels of aspartate aminotransferase, total bilirubin, IL-1ß, IL-6, TNF-a, and malondialdehyde. Plasma albumin, total protein, total antioxidant capacity and glutathione peroxidase decreased post-challenge. The results were better with OH-Met than DL-Met. The increase of Met consumption, particularly as OH-Met increased piglets' growth performance during the lactation phase and the challenging period.

Effects of recombinant Agrocybe aegerita lectin as an immunoadjuvant on immune responses.

CONTEXT: Accumulated evidence has indicated that recombinant Agrocybe aegerita lectin (AAL) possesses immunoadjuvant activity to enhance antigen-specific immune responses. However, the mechanism of how AAL regulates immune response remains poorly defined. AIM: This study is aimed to reveal the mechanism of AAL's immunoadjuvant activity. METHODS: In this study, AAL alone or combined with inactivated avian influenza virus H9N2 was immunized to mice and the transcriptome profile of immunized mice was analyzed. RESULTS: In line with previous studies, our results showed that H9N2-specific IgG level was significantly increased in AAL-treated mice, suggesting the immunoadjuvant activity of AAL. More importantly, transcriptome data revealed that genes participating in the primary adherence, lymphocyte activation, secondary adherence and transmembrane migration of leukocyte migration, were up-regulated by AAL. CONCLUSION: These findings suggest that AAL exerts immunoadjuvant effects by promoting chemotaxis and phagotrophy activity of neutrophil leucocyte and macrophage to improve innate immunity and antigen presentation.

Adjuvant effects mediated by the carbohydrate recognition domain of Agrocybe aegerita lectin interacting with avian influenza H9N2 viral surface glycosylated proteins.

OBJECTIVE: To evaluate the potential adjuvant effect of Agrocybe aegerita lectin (AAL), which was isolated from mushroom, against a virulent H9N2 strain in vivo and in vitro. METHODS: In trial 1, 50 BALB/c male mice (8 weeks old) were divided into five groups (n=10 each group) which received a subcutaneous injection of inactivated H9N2 (control), inactivated H9N2+0.2% (w/w) alum, inactivated H9N2+0.5 mg recombinant AAL/kg body weight (BW), inactivated H9N2+1.0 mg AAL/kg BW, and inactivated H9N2+2.5 mg AAL/kg BW, respectively, four times at 7-d intervals. In trial 2, 30 BALB/c male mice (8 weeks old) were divided into three groups (n=10 each group) which received a subcutaneous injection of inactivated H9N2 (control), inactivated H9N2+2.5 mg recombinant wild-type AAL (AAL-wt)/kg BW, and inactivated H9N2+2.5 mg carbohydrate recognition domain (CRD) mutant AAL (AAL-mutR63H)/kg BW, respectively, four times at 7-d intervals. Seven days after the final immunization, serum samples were collected from each group for analysis. Hemagglutination assay, immunogold electron microscope, lectin blotting, and co-immunoprecipitation were used to study the interaction between AAL and H9N2 in vitro. RESULTS: IgG, IgG1, and IgG2a antibody levels were significantly increased in the sera of mice co-immunized with inactivated H9N2 and AAL when compared to mice immunized with inactivated H9N2 alone. No significant increase of the IgG antibody level was detected in the sera of the mice co-immunized with inactivated H9N2 and AAL-mutR63H. Moreover, AAL-wt, but not mutant AAL-mutR63H, adhered to the surface of H9N2 virus. The interaction between AAL and the H9N2 virus was further demonstrated to be associated with the CRD of AAL binding to the surface glycosylated proteins, hemagglutinin and neuraminidase. CONCLUSIONS: Our findings indicated that AAL could be a safe and effective adjuvant capable of boosting humoral immunity against H9N2 viruses in mice through its interaction with the viral surface glycosylated proteins, hemagglutinin and neuraminidase.