Search

To elucidate the function of type II ice structuring protein (ISP II) in the cold tolerance and resistance of Ruditapes philippinarum , we investigated ISP II mRNA expression, the antifreeze effect of recombinant ISP II protein, and adaptation of R. philippinarum after acute and chronic cold stress. Bacterial freeze-thaw experiments showed that ISP II significantly increased the survival rate of Escherichia coli BL21 (DE3) under low temperature stress, suggesting that it had a potential antifreeze effect. Furthermore, rISP II protein injections significantly increased the survival rate of R. philippinarum compared with a PBS control group. In addition, succinate dehydrogenase (SDH), lactate dehydrogenase (LDH), and glutathione peroxidase (GSH-Px) activities, Malondialdehyde (MDA) content, total antioxidant capacity (T-AOC), and immune-related genes (Syk, SCD , and SOD) were measured in three populations of clams (northern, southern, and zebra). The results indicated that ISP II was likely to improve the cold resistance and performance of R. philippinarum under cold stress. These results not only provided molecular insights for improving the low-temperature resistance and immunity of shellfish but also provided useful information for improving the low temperature tolerance of R. philippinarum in aquaculture environments. • ISP II was likely to enhance the cold resistance of R. philippinarum under low temperature. • The rISP II injection experiments verified the potential role in low temperature tolerance of ISP II. • The zebra strains probably have a better potential for breeding cold resistance in Manila clams. [ABSTRACT FROM AUTHOR]

The therapeutic application of antimicrobial peptides (AMPs), a potential type of peptide-based biomaterial, is impeded by their poor antimicrobial activity and potential cytotoxicity as a lack of understanding of their structure–activity relationships. In order to comprehensively enhance the antibacterial and clinical application potency of AMPs, a rational approach was applied to design amphiphilic peptides, including head-to-tail cyclic, linear and D-proline antimicrobial peptides using the template (IR)nP(IR)nP (n = 1, 2 and 3). Results showed that these amphiphilic peptides demonstrated antimicrobial activity in a size-dependent manner and that cyclic peptide OIR3, which contained three repeating units (IR)3, had greater antimicrobial potency and cell selectivity than liner peptide IR3, DIR3 with D-Pro and gramicidin S (GS). Surface plasmon resonance and endotoxin neutralization assays indicated that OIR3 had significant endotoxin neutralization capabilities, which suggested that the effects of OIR3 were mediated by binding to lipopolysaccharides (LPS). Using fluorescence spectrometry and electron microscopy, we found that OIR3 strongly promoted membrane disruption and thereby induced cell lysis. In addition, an LPS-induced inflammation assay showed that OIR3 inhibited the pro-inflammatory factor TNF-α in RAW264.7 cells. OIR3 was able to reduce oxazolone-induced skin inflammation in allergic dermatitis mouse model via the inhibition of TNF-α, IL-1β and IL-6 mRNA expression. Collectively, the engineered head-to-tail cyclic peptide OIR3 was considerable potential candidate for use as a clinical therapeutic for the treatment of bacterial infections and skin inflammation. [ABSTRACT FROM AUTHOR]

Antibacterial peptides (APMs) are a new type of antibacterial substance. The relationship between their structure and function remains indistinct; in particular, there is a lack of a definitive and fixed template for designing new antimicrobial peptides. Previous studies have shown that porcine Protegrin-1 (PG-1) exhibits considerable antimicrobial activity and cytotoxicity. In this study, to reduce cytotoxicity and increase cell selectivity, we designed histidine-rich peptides based on the sequence template RR(XY)2XDPGX(YX)2RR-NH2, where X represents I, W, V, and F. The results showed that the peptides form more β-hairpin structures in a lipid-rich environment that mimics cell membranes. Among them, the antimicrobial peptide HV2 showed strong antibacterial activity against Gram-negative strains and almost no toxicity to normal cells. The results of our analysis of its antibacterial mechanism showed that peptide HV2 acts on the bacterial cell membrane to increase its permeability, resulting in cell membrane disruption and death. Furthermore, peptide HV2 inhibited bacterial movement in a concentration-dependent manner and had a more robust anti-inflammatory effect by inhibiting the production of TNF-α. In summary, peptide HV2 exhibits high bactericidal activity and cell selectivity, making it a promising candidate for future use as an antibiotic. [ABSTRACT FROM AUTHOR]

Early weaning usually causes intestinal disorders, enteritis, and diarrhea in young animals and human infants. Astragalus polysaccharides (APS) possesses anti‐inflammatory activity. To study the anti‐inflammatory mechanisms of APS and its potential effects on intestinal health, we performed an RNA sequencing (RNA‐seq) study in lipopolysaccharide (LPS)‐stimulated porcine intestinal epithelial cells (IPEC‐J2) in vitro. In addition, LPS‐stimulated BALB/c mice were used to study the effects of APS on intestinal inflammation in vivo. The results from the RNA‐seq analysis show that there were 107, 756, and 5 differentially expressed genes in the control versus LPS, LPS versus LPS+APS, and control versus LPS+APS comparison groups, respectively. The results of Kyoto Encyclopedia of Genes and Genomes enrichment analysis indicated that the mitogen‐activated protein kinase (MAPK) and nuclear factor‐κB (NF‐κB) signaling pathways play significant roles in the regulation of inflammatory factors and chemokine expression by APS. Further verification of the above two pathways by using western blot and immunofluorescence analysis revealed that the gene expression levels of the phosphorylated p38 MAPK, ERK1/2, and NF‐κB p65 were inhibited by APS, while the expression of IκB‐α protein was significantly increased (p <.05), indicating that APS inhibits the production of inflammatory factors and chemokines by the inhibition of activation of the MAPK and NF‐κB inflammatory pathways induced by LPS stimulation. Animal experiments further demonstrated that prefeeding APS in BALB/c mice can alleviate the expression of the jejunal inflammatory factors interleukin 6 (IL‐6), IL‐Iβ, and tumor necrosis factor‐α induced by LPS stimulation and improve jejunal villus morphology. [ABSTRACT FROM AUTHOR]

Salmonella typhimurium is one of the main causes of intestinal diseases, affecting the health of humans and livestock. Ethyl pyruvate (EP), which is ordinarily an edible spice, has been indicated to exert anti-inflammatory effects and preserve intestinal barrier function. In this study, intestinal immune function and signaling pathways activated by EP were investigated in vivo in S. typhimurium- challenged BALB/c mice and in vitro in RAW264.7 cells. EP improved body weight loss and the organ index of the liver and spleen (p < 0.05). Serum IgA and IgM levels were significantly increased in EP-treated mice (p < 0.05). According to histopathological and immunohistochemical staining, EP significantly increased the villus height, reduced edema in the jejunum and increased the levels of claudin-1, occludin-1 and ZO-1 proteins compared to the Salmonella -treated group (p < 0.05). In addition, EP decreased the levels of the IL-6, IL-1β and TNF-α mRNA levels in jejunum, liver, spleen and RAW264.7 cells (p < 0.05). EP decreased the levels of TLR4, phosphorylated p38MAPK and ERK1/2 in mice infected with S. typhimurium (p < 0.05). In conclusion, EP effectively protected BALB/c mice from an intestinal S. typhimurium infection by improving the activity of the humoral immune system, reducing intestinal barrier damage, and inhibiting proinflammatory cytokine production in the jejunum by modulating the TLR4/MAPK signaling pathway. Based on these findings, EP has the potential to inhibit inflammation or to serve as an immune-enhancing adjuvant. [ABSTRACT FROM AUTHOR]

This review aims to provide an overview of the sources and reactions of persistent organic pollutants (POPs) and surfactants in soil and sediments, the surfactant-enhanced solubilisation of POPs, and the unintended consequences of surfactant-induced remediation of soil and sediments contaminated with POPs. POPs include chemical compounds that are recalcitrant to natural degradation through photolytic, chemical, and biological processes in the environment. POPs are potentially toxic compounds mainly used in pesticides, solvents, pharmaceuticals, or industrial applications and pose a significant and persistent risk to the ecosystem and human health. Surfactants can serve as detergents, wetting and foaming compounds, emulsifiers, or dispersants, and have been used extensively to promote the solubilization of POPs and their subsequent removal from environmental matrices, including solid wastes, soil, and sediments. However, improper use of surfactants for remediation of POPs may lead to unintended consequences that include toxicity of surfactants to soil microorganisms and plants, and leaching of POPs, thereby resulting in groundwater contamination. [Display omitted] • POPs include organic compounds that are resistant to natural environmental degradation. • Surfactants form micelles in solution and are effective in the solubilization of POPs. • Surfactants enhance remediation via soil washing, bioremediation, and phytoremediation. • Provided case studies for surfactant-induced remediation of POPs. • Demonstrated unintended consequences of surfactant-induced remediation of POPs. [ABSTRACT FROM AUTHOR]

Salmonella typhimurium (S. t.) is one of the main pathogens that causes acute gastroenteritis. To evaluate the anti-inflammatory mechanism of Astragalus polysaccharide (APS) in vivo and its influence on the intestinal flora, BALB/c mice were infected with S. t. to establish a model of diarrhea. The disease activity index (DAI) scores showed that APS attenuated S. t.-induced weight loss and diarrhea in mice. APS significantly reduced the index of the liver and spleen as well as the ALT and AST levels in serum (P < 0.05). Hematoxylin and eosin (H&E) results indicated that APS significantly increased jejunum villus height and crypt depth and reduced the infiltration of inflammatory cells (P < 0.05). Additionally, APS increased the tight junction (TJ) proteins expression levels of ZO-1, Occludin and Claudin-1 in the jejunum. The results of 16S rDNA showed that APS significantly increased the number of Lactobacillus and Bifidobacterium spp. to normal levels (compared with the control group). In addition, APS significantly decreased the mRNA expression levels of the proinflammatory cytokines TNF-α, IL-1β, IL-6 and IL-17 in the jejunum (P < 0.01) as well as the proteins expression levels of COX-2 and iNOS (P < 0.05). Western blot confirmed that prefeeding with APS inhibited S. t. -induced expression of TLR4 and MyD88 in the jejunum and further inhibited nuclear factor-κB (NF-κB) activation, including the nuclear translocation of the p65 NF-κB subunit and the phosphorylation and degradation of IκB-α. This was the key to APS inhibition of the production of inflammatory factors and inflammatory mediators in the jejunum. • In our study, APS relieved inflammation through inhibiting body weight loss and reducing the liver and spleen index of infected mice. • APS increased the intestinal barrier function by repairing damaged structures of the jejunum villi and balancing intestinal flora. • PS is expected to be an alternative to antibiotics for the treatment of intestinal inflammation caused by bacterial infections. [ABSTRACT FROM AUTHOR]