Dihydroartemisinin ameliorates innate inflammatory response induced by -derived muramidase-released protein via inactivation of TLR4-dependent NF-κB signaling.

Muramidase-released protein (MRP) is now being recognized as a critical indicator of the virulence and pathogenicity of (). However, the identification of viable therapeutics for infection was hindered by the absence of an explicit mechanism for MRP-actuated inflammation. Dihydroartemisinin (DhA) is an artemisinin derivative with potential anti-inflammatory activity.

Intersex is required for female sexual development in Hermetia illucens.

Sex-determination pathways are extremely diverse. Understanding the mechanism of sex determination in insects is important for genetic manipulation of the pest population and for breeding of economically valuable insects. Although sex determination has been well characterized in the model species Drosophila melanogaster, little is known about this pathway in Stratiomyidae.

Dietary l-Tryptophan Supplementation Enhances the Intestinal Mucosal Barrier Function in Weaned Piglets: Implication of Tryptophan-Metabolizing Microbiota.

l-Tryptophan (Trp) is known to play an important role in the health of the large intestine. However, a role of dietary Trp in the small-intestinal mucosal barrier and microbiota remains poorly understood. The present study was conducted with weaned piglets to address this issue.

S100A4 protects mice from high-fat diet-induced obesity and inflammation.

As a member from S100 calcium-binding protein family, S100A4 is ubiquitous and elevated in tumor progression and metastasis, but its role in regulating obesity has not been well characterized. In this study, we showed that S100A4 was mainly expressed by stromal cells in adipose tissue and the S100A4 level in adipose tissue was decreased after high-fat diet (HFD). S100A4 deficient mice exhibited aggravated symptoms of obesity and suppressed insulin signaling after 12 weeks of HFD.

S100A4 promotes lung tumor development through β-catenin pathway-mediated autophagy inhibition.

Autophagy has emerged as a critical pathway in tumor development. S100A4 plays important roles in tumor metastasis, but its role in regulating autophagy has not been well characterized. In this study, we found that S100A4 was significantly upregulated in lung adenocarcinoma tissues.

Intestinal Epithelial Cell Endoplasmic Reticulum Stress and Inflammatory Bowel Disease Pathogenesis: An Update Review.

The intestinal epithelial cells serve essential roles in maintaining intestinal homeostasis, which relies on appropriate endoplasmic reticulum (ER) function for proper protein folding, modification, and secretion. Exogenous or endogenous risk factors with an ability to disturb the ER function can impair the intestinal barrier function and activate inflammatory responses in the host. The last decade has witnessed considerable progress in the understanding of the functional role of ER stress and unfolded protein response (UPR) in the gut homeostasis and its significant contribution to the pathogenesis of inflammatory bowel disease (IBD).

Interactions between Intestinal Microbiota and Host Immune Response in Inflammatory Bowel Disease.

Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract. Although the etiology and pathogenesis of IBD remain unclear, both genetic susceptibility and environmental factors are implicated in the initiation and progression of IBD. Recent studies with experimental animal models and clinical patients indicated that the intestinal microbiota is one of the critical environmental factors that influence nutrient metabolism, immune responses, and the health of the host in various intestinal diseases, including ulcerative colitis and Crohn's disease.

Cinnamicaldehyde regulates the expression of tight junction proteins and amino acid transporters in intestinal porcine epithelial cells.

Background: Cinnamicaldehyde (CA) is a key flavor compound in cinnamon essential oil possessing various bioactivities. Tight junction (TJ) proteins are vital for the maintenance of intestinal epithelial barrier function, transport, absorption and utilization of dietary amino acids and other nutrients. In this study, we tested the hypothesis that CA may regulate the expression of TJ proteins and amino acid transporters in intestinal porcine epithelial cells (IPEC-1) isolated from neonatal pigs.

Glycine Regulates Protein Turnover by Activating Protein Kinase B/Mammalian Target of Rapamycin and by Inhibiting MuRF1 and Atrogin-1 Gene Expression in C2C12 Myoblasts.

Background: The regulation of protein turnover in skeletal muscle is essential for the maintenance of integrity, growth, and function of this tissue. We recently reported that glycine enhances skeletal muscle growth in young pigs. However, the underlying mechanisms remain unknown.

Glycine Regulates Expression and Distribution of Claudin-7 and ZO-3 Proteins in Intestinal Porcine Epithelial Cells.

Background: Glycine traditionally is classified as a nutritionally nonessential amino acid in humans and animals. Because of its abundance in the body and its extensive use via multiple pathways, requirements for glycine are particularly high in neonates. Our recent studies show that dietary glycine supplementation is needed for optimal intestinal development in piglets.

L-Glutamine Enhances Tight Junction Integrity by Activating CaMK Kinase 2-AMP-Activated Protein Kinase Signaling in Intestinal Porcine Epithelial Cells.

Background: The tight junctions (TJs) are essential for maintenance of the intestinal mucosal barrier integrity. Results of our recent work show that dietary l-glutamine (Gln) supplementation enhances the protein abundance of TJ proteins in the small intestine of piglets. However, the underlying mechanisms remain largely unknown.

Nutritional epigenetics with a focus on amino acids: implications for the development and treatment of metabolic syndrome.

Recent findings from human and animal studies indicate that maternal undernutrition or overnutrition affects covalent modifications of the fetal genome and its associated histones that can be carried forward to subsequent generations. An adverse outcome of maternal malnutrition is the development of metabolic syndrome, which is defined as a cluster of disorders including obesity, hyperglycemia, hyperinsulinemia, hyperlipidemia, hypertension and insulin resistance. The transgenerational impacts of maternal nutrition are known as fetal programming, which is mediated by stable and heritable alterations of gene expression through covalent modifications of DNA and histones without changes in DNA sequences (namely, epigenetics).

Intimacy and a deadly feud: the interplay of autophagy and apoptosis mediated by amino acids.

Autophagy (i.e., "self-eating") and apoptosis (i.

Excessive L-cysteine induces vacuole-like cell death by activating endoplasmic reticulum stress and mitogen-activated protein kinase signaling in intestinal porcine epithelial cells.

High intake of dietary cysteine is extremely toxic to animals and the underlying mechanism remains largely unknown. This study was conducted to test the hypothesis that excessive L-cysteine induces cell death by activating endoplasmic reticulum (ER) stress and mitogen-activated protein kinase (MAPK) signaling in intestinal porcine epithelial cells. Jejunal enterocytes were cultured in the presence of 0-10 mmol/L L-cysteine.

Dietary L-leucine supplementation enhances intestinal development in suckling piglets.

L-Leucine is a signaling amino acid in animal metabolism. It is unknown whether supplementing L-leucine to breast-fed neonates may enhance their small-intestinal development. This hypothesis was tested with a piglet model.

l-Tryptophan Activates Mammalian Target of Rapamycin and Enhances Expression of Tight Junction Proteins in Intestinal Porcine Epithelial Cells.

Background: Besides serving as a substrate for protein synthesis, L-tryptophan (L-Trp) is used via serotonin-, kynurenine-, and niacin-synthetic pathways to produce bioactive compounds crucial for whole-body homeostasis. It is unknown whether L-Trp itself can regulate metabolic pathways in animal cells.

Objective: This study tested the hypothesis that L-Trp may activate mammalian target of rapamycin (mTOR) complex 1 and enhance expression of tight junction (TJ) proteins in intestinal porcine epithelial cells.

Dietary L-methionine restriction decreases oxidative stress in porcine liver mitochondria.

Dietary methionine restriction (MetR) has been reported to improve hepatocyte function in mammals. However, the underlying mechanisms remain largely unknown. This study was conducted with a swine model to test the hypothesis that MetR decreases generation of reactive oxygen species (ROS) and attenuates oxidative damage in hepatic mitochondria.