Comprehensive strategies for controlling Listeria monocytogenes biofilms on food-contact surfaces.

Listeria monocytogenes biofilms formed on food-contact surfaces within food-processing facilities pose a significant challenge, serving as persistent sources of cross-contamination. In this review, we examined documented cases of foodborne outbreaks and recalls linked to L. monocytogenes contamination on equipment surfaces and in the food production environment, provided an overview of the prevalence and persistence of L. monocytogenes in different food-processing facilities, and discussed environmental factors influencing its biofilm formation. We further delved into antimicrobial interventions, such as chemical sanitizers, thermal treatments, biological control, physical treatment, and other approaches for controlling L. monocytogenes biofilms on food-contact surfaces. This review provides valuable insights into the persistent challenge of L. monocytogenes biofilms in food processing, offering a foundation for future research and practical strategies to enhance food safety.

α-Ketoglutarate for Preventing and Managing Intestinal Epithelial Dysfunction.

The epithelium lining the intestinal tract serves a multifaceted role. It plays a crucial role in nutrient absorption and immune regulation and also acts as a protective barrier, separating underlying tissues from the gut lumen content. Disruptions in the delicate balance of the gut epithelium trigger inflammatory responses, aggravate conditions such as inflammatory bowel disease, and potentially lead to more severe complications such as colorectal cancer. Maintaining intestinal epithelial homeostasis is vital for overall health, and there is growing interest in identifying nutraceuticals that can strengthen the intestinal epithelium. α-Ketoglutarate, a metabolite of the tricarboxylic acid cycle, displays a variety of bioactive effects, including functioning as an antioxidant, a necessary cofactor for epigenetic modification, and exerting anti-inflammatory effects. This article presents a comprehensive overview of studies investigating the potential of α-ketoglutarate supplementation in preventing dysfunction of the intestinal epithelium.

AMPK Suppression Due to Obesity Drives Oocyte mtDNA Heteroplasmy via ATF5-POLG Axis.

Due to the exclusive maternal transmission, oocyte mitochondrial dysfunction reduces fertility rates, affects embryonic development, and programs offspring to metabolic diseases. However, mitochondrial DNA (mtDNA) are vulnerable to mutations during oocyte maturation, leading to mitochondrial nucleotide variations (mtSNVs) within a single oocyte, referring to mtDNA heteroplasmy. Obesity (OB) accounts for more than 40% of women at the reproductive age in the USA, but little is known about impacts of OB on mtSNVs in mature oocytes. It is found that OB reduces mtDNA content and increases mtSNVs in mature oocytes, which impairs mitochondrial energetic functions and oocyte quality. In mature oocytes, OB suppresses AMPK activity, aligned with an increased binding affinity of the ATF5-POLG protein complex to mutated mtDNA D-loop and protein-coding regions. Similarly, AMPK knockout increases the binding affinity of ATF5-POLG proteins to mutated mtDNA, leading to the replication of heteroplasmic mtDNA and impairing oocyte quality. Consistently, AMPK activation blocks the detrimental impacts of OB by preventing ATF5-POLG protein recruitment, improving oocyte maturation and mitochondrial energetics. Overall, the data uncover key features of AMPK activation in suppressing mtSNVs, and improving mitochondrial biogenesis and oocyte maturation in obese females.

Evaluation of Enterococcus faecium NRRL B-2354 as a surrogate for Listeria monocytogenes during chlorine and peroxyacetic acid interventions in simulated apple dump tank water.

Sanitizers are widely incorporated in commercial apple dump tank systems to mitigate the cross-contamination of foodborne pathogens. This study validated the suitability of Enterococcus faecium NRRL B-2354 as a surrogate for Listeria monocytogenes during sanitizer interventions in dump tank water systems. E. faecium NRRL B-2354 inoculated on apples exhibited statistically equivalent susceptibility to L. monocytogenes when exposed to chlorine-based sanitizers (25-100 ppm free chlorine (FC)) and peroxyacetic acid (PAA, 20-80 ppm) in simulated dump tank water (SDTW) with 1000 ppm chemical oxygen demand (COD), resulting in 0.2-0.9 and 1.1-1.7 log CFU/apple reduction, respectively. Increasing the contact time did not affect sanitizer efficacies against E. faecium NRRL B-2354 and L. monocytogenes on apples. Chlorine and PAA interventions demonstrated statistically similar efficacies against both bacteria inoculated in SDTW. Chlorine at 25 and 100 ppm FC for 0.5-5 min contact yielded ~37.68-78.25 % and > 99.85 % inactivation, respectively, in water with 1000-4000 ppm COD, while ~51.55-99.86 % and > 99.97 % inactivation was observed for PAA at 20 and 80 ppm, respectively. No statistically significant difference was observed between the transference of E. faecium NRRL B-2354 and L. monocytogenes from inoculated apples to uninoculated apples and water, and from water to uninoculated apples during chlorine- or PAA-treated SDTW exposure. The data suggest E. faecium NRRL B-2354 is a viable surrogate for L. monocytogenes in dump tank washing systems, which could be used to predict the anti-Listeria efficacy of chlorine and PAA interventions during commercial apple processing. Further investigations are recommended to assess the suitability of E. faecium NRRL B-2354 as a surrogate for L. monocytogenes, when using different sanitizers and different types of produce to ensure reliable and comprehensive results.

Impacts of water activity on survival of Listeria innocua and Enterococcus faecium NRRL B-2354 in almonds during steam treatments.

Raw almonds have been associated with Salmonella outbreaks and multiple recalls related to Listeria monocytogenes contamination. While steam treatment has been approved for pasteurizing both conventional and organic whole almonds, there is limited understanding of how water activity (aw) influences the effectiveness of steam treatments in decontaminating almonds. Hence, this study aimed to assess and compare the efficacy of steam treatments against Listeria innocua and Enterococcus faecium NRRL B-2354, the known non-pathogenic surrogates, on almonds. It also sought to investigate the impact of almond's aw on bacterial resistance during steam treatments. Almond kernels were inoculated with ~8 log10 CFU/g of either E. faecium or L. innocua and equilibrated to aw 0.25 or 0.45 before being subjected to steam treatments at temperatures of 100-135 °C. Our results revealed that L. innocua exhibited lower resistance to steam compared to E. faecium, with 1.2-2.6 log10 CFU/g reductions for L. innocua and 1.0-2.0 log10 CFU/g reductions for E. faecium when the surface temperature of almonds reached 100-130 °C, depending on the aw of the almonds. The obtained DL. innocua, 100-130°C-values were 2.0-16.6 s, and DE. faecium, 100-130°C-values were 4.0-21.8 s, depending on the aw of almonds. In general, elevating steam temperatures and almond aw decreased the tolerance of L. innocua and E. faecium during steam inactivation. In addition, the z-values indicated that E. faecium on almonds was less sensitive to change in steam temperature compared to L. innocua, especially at lower aw. The zL. innocua-values were 36.6 °C and 35.7 °C, while zE. faecium-values were 48.9 °C and 42.7 °C in almonds with aw 0.25 and 0.45, respectively. Results from this study suggest that steam treatments serve as effective interventions for controlling pathogen contaminations in raw almonds.

Dietary Cannabidiol Activates PKA/AMPK Signaling and Attenuates Chronic Inflammation and Leaky Gut in DSS-Induced Colitis Mice.

SCOPE: Inflammatory bowel disease (IBD) is characterized by chronic inflammation in the gut, accompanied by impaired epithelial integrity, increased macrophage infiltration, and enhanced colon cancer risk. METHODS AND RESULTS: Cannabidiol (CBD), a phytocannabinoid isolated from cannabis plants, is supplemented into mice diet, and its beneficial effects against dextran sulfate sodium (DSS)-induced experimental colitis is evaluated. Eight-week-old mice were fed a standard diet supplemented with or without CBD (200 mg kg-1 ) for 5 weeks. In the 4th week of dietary treatment, mice were subjected to 2.5% DSS induction for 7 days, followed by 7 days of recovery, to induce colitis. CBD supplementation reduced body weight loss, gross bleeding, fecal consistency, and disease activity index. In addition, CBD supplementation protected the colonic structure, promoted tissue recovery, and ameliorated macrophage infiltration in the colonic tissue, which was associated with the activation of cyclic AMP-protein kinase A, extracellular signal-regulated kinase ½, and AMP-activated protein kinase signaling pathways. CBD supplementation also suppressed NLRP3 inflammasome activation and related pro-inflammatory marker secretion. Consistently, CBD feeding reduced tight junction protein claudin2 and myosin light chain kinase in DSS-treated mice. CONCLUSION: Dietary CBD protects against inflammation and colitis symptoms induced by DSS, providing an alternative approach to IBD management.

Unlocking the Hidden Threat: Impacts of Surface Defects on the Efficacy of Sanitizers Against Listeria monocytogenes Biofilms on Food-contact Surfaces in Tree Fruit Packing Facilities.

Food-contact surfaces showing signs of wear pose a substantial risk of Listeria monocytogenes contamination and may serve as persistent sources of cross-contamination in fresh produce packinghouses. This study offers a comprehensive exploration into the influence of surface defects on the efficacies of commonly used sanitizers against L. monocytogenes biofilms on major food-contact surfaces. The 7-day-old L. monocytogenes biofilms were cultivated on food-contact surfaces, including stainless steel, polyvinyl chloride, polyester, low-density polyethylene, and rubber, with and without defects and organic matter. Biofilms on those surfaces were subjected to treatments of 200 ppm chlorine, 400 ppm quaternary ammonium compound (QAC), or 160 ppm peroxyacetic acid (PAA). Results showed that surface defects significantly (P < 0.05) increased the population of L. monocytogenes in biofilms on non-stainless steel surfaces and compromised the efficacies of sanitizers against L. monocytogenes biofilms across various surface types. A 5-min treatment of 200 ppm chlorine caused 1.84-3.39 log10 CFU/coupon reductions of L. monocytogenes on worn surfaces, compared to 2.79-3.93 log10 CFU/coupon reduction observed on new surfaces. Similarly, a 5-min treatment with 400 ppm QAC caused 2.05-2.88 log10 CFU/coupon reductions on worn surfaces, compared to 2.51-3.66 log10 CFU/coupon reductions on new surfaces. Interestingly, PAA sanitization (160 ppm, 1 min) exhibited less susceptibility to surface defects, leading to 3.41-4.35 log10 CFU/coupon reductions on worn surfaces, in contrast to 3.68-4.64 log10 CFU/coupon reductions on new surfaces. Furthermore, apple juice soiling diminished the efficacy of sanitizers against L. monocytogenes biofilms on worn surfaces (P < 0.05). These findings underscore the critical importance of diligent equipment maintenance and thorough cleaning processes to effectively eliminate L. monocytogenes contamination on food-contact surfaces.

Dietary purple potato supplement attenuates DSS-induced colitis in mice: impact on mitochondrial function.

Inflammatory bowel disease (IBD) is a condition characterized by disrupted intestinal barrier function, abnormal immune response, and mucosal structure loss. This study evaluated the beneficial role of purple potato (PP) supplementation against IBD symptoms using a murine model of dextran sulfate sodium (DSS)-induced colitis, and further explored the underlying mechanisms. Six-week-old C57BL/6J male mice were randomized into two groups and fed a standard rodent diet with or without 10% PP powder for 7 weeks. At the 5th week of dietary supplements, mice in each group were further divided into two subgroups and were either induced with or without 2.5% DSS induction for 7 days, followed by 7 days of recovery. Data showed that PP supplementation ameliorated the disease activity index in DSS-treated mice and reversed the colonic structure loss, mucosal damage, macrophage infiltration, and pro-inflammatory cytokine secretion induced by DSS in the colonic tissue. PP supplementation also restored the levels of tight junction proteins and caudal type homeobox 2 in DSS-treated mice. Furthermore, dietary PP enhanced peroxisome proliferator-activated receptor-γ coactivator-1α signaling pathway, mitochondrial biogenesis, mitochondrial proteostasis, and protein-folding capacity. In summary, dietary PP ameliorated DSS-induced colitis and improved gut structures and barrier function, which was associated with improved mitochondrial function. These results support further investigation of PP as a potential dietary intervention for IBD.

Exercise enhances placental labyrinth trophoblast development by activation of PGC-1α and FNDC5/irisin†.

Placental chorion/labyrinth trophoblasts are energy demanding which is met by the mitochondrial oxidative phosphorylation. Exercise enhances placental development and mitochondrial biogenesis, but the underlying mechanisms remain poorly understood. To address, female C57BL/6 J mice were randomly assigned into two groups: a control group and an exercise (EX) group. All animals were acclimated to treadmill exercise for 1 week before mating, but only the EX group was subjected to daily exercise during pregnancy from embryonic day (E) 1.5 to E16.5. Placenta were collected at E18.5 for biochemical and histochemical analyses, and primary trophoblast cells were isolated from the E18.5 placenta for further analyses. The data showed that exercise during pregnancy promoted the expression of syncytiotrophoblast cell markers, indicating trophoblast cell differentiation, which was closely associated with elevated mitochondrial biogenesis and oxidative metabolism in the E18.5 placenta. In addition, exercise during pregnancy activated peroxisome proliferator-activated receptor γ coactivator-1 α (PGC-1α), which was associated with upregulated placental α-ketoglutarate and the expression of isocitrate dehydrogenases and ten-eleven translocations, facilitating DNA demethylation of the Pgc1a promoter. Furthermore, exercise upregulated fibronectin type III domain containing 5 expression and the secretion of its cleaved form, irisin, which is known to activate PGC-1α. These data suggest that exercise-induced activation of PGC-1α, via epigenetic modifications, is responsible for promoting mitochondrial energy metabolism and chorion/labyrinth trophoblast development.

Enhancing the efficacy of peracetic acid against Listeria monocytogenes and Listeria innocua on fresh apples using commercial acidic and alkaline cleaners.

Peracetic acid (PAA) is a commonly used antimicrobial in brush-bed spray bar interventions during apple packing. Prior to sanitizer application on the brush-bed, specific fruit cleaners, such as Acidex Duo (AD), EpiClean (EC), Nature's Shield 220-ACL (NS 220), or Nature's Shield 330-ALK (NS 330), are used to remove of soil, debris, and natural wax from the surfaces of apples. This study evaluated the effectiveness of commonly used cleaners in the apple industry to improve the antimicrobial efficacy of PAA against Listeria monocytogenes on apple surfaces during brush-bed spray bar interventions. Granny Smith apples, 48 h post-inoculation, underwent submersion treatment with different cleaners, as well as PAA alone or in combination with the cleaners. A 30-sec treatment of 5.0% AD, 4.2% EC, 10.0% NS 220, and 10.0% NS 330 resulted in 0.65, 0.50, 0.68, and 0.51 log10 CFU/apple reduction of L. monocytogenes on apples, respectively. Incorporating AD, NS 220, and EC significantly enhanced the antimicrobial efficacy of an 80 ppm PAA intervention. The enhancing effects were not impacted whether the cleaner was applied consecutively with PAA (sequentially) or in combination with PAA (simultaneously), nor were they impacted by a post-treatment water rinse. A 30-120 s wash of 80 ppm PAA with AD, EC, and NS 220 at their suggested concentration resulted in 2.46-2.55, 1.87-2.03, and 2.34-2.48 log10 CFU/apple reduction of L. monocytogenes, respectively, compared to 1.39-1.64 log10 CFU/apple in PAA treatment alone. The inclusion of AD or NS 220 in 80 ppm PAA solution resulted in a reduction of 1.51-1.63 log10 CFU/apple of Listeria after 30-60 s brush-bed spray wash. This enhancement in efficacy was significant compared to the treatment with 80 ppm PAA alone, which resulted in a reduction of 0.94-1.03 log10 CFU/apple. This study demonstrated that using certain commercially available cleaners along with PAA can enhance the effectiveness of PAA in reducing L. monocytogenes on fresh apples.

Survival and thermal resistance of Salmonella in chocolate products with different water activities.

Contamination of Salmonella in chocolate products has caused worldwide outbreaks and recalls. There is a lack of information on the impact of water activity (aw) on the stability of Salmonella in chocolate products during storage and thermal treatments. In this research, the survival and thermal resistance of a Salmonella cocktail (S. Enteritidis PT30, S. Tennessee K4643, S. Typhimurium S544) was examined in different chocolate products (dark chocolate, white chocolate, milk chocolate) at two aw levels (0.25, 0.50) over 12 months at 22 °C. A reduction of 4.19 log10 CFU/gof Salmonella was obtained in dark chocolate after 12 months (aw = 0.50, at 22 °C); less reductions were observed in white and milk chocolates. In all three products, more reductions were observed ataw = 0.50 than at aw = 0.25 over the 12-months storage. When treated at 80 °C, the D-values (time required to cause 1 log reduction) of the Salmonella cocktail in the chocolate samples with initial aw of 0.25 were 35.7, 25.2 and 11.6 min in dark, white and milk chocolate, respectively, before the storage. The D80°C -values of Salmonella cocktail in the samples with initial aw of 0.50 were 6.45, 7.46, and 3.98 min in dark, white and milk chocolate, respectively. After 12 months of storage at 22 °C, the D80°C-value of Salmonella cocktail decreased to 9.43 min (p < 0.05) in milk chocolate but remained 22.7 min in white chocolate with an aw of 0.25 at 22 °C. The data suggests that Salmonella can survive in chocolate products for up to 12 months, and its thermal resistance remained relatively stable. Thus, Salmonella is resistant to desiccation in chocolates, particularly in milk and white chocolates, and its thermal resistance remains during one-year storage, which could pose a potential threat for future outbreaks.

Exercise improves homeostasis of the intestinal epithelium by activation of apelin receptor-AMP-activated protein kinase signalling.

Intestinal remodelling is dynamically regulated by energy metabolism. Exercise is beneficial for gut health, but the specific mechanisms remain poorly understood. Intestine-specific apelin receptor (APJ) knockdown (KD) and wild-type male mice were randomly divided into two subgroups, with/without exercise, to obtain four groups: WT, WT with exercise, APJ KD and APJ KD with exercise. Animals in the exercise groups were subjected to daily treadmill exercise for 3 weeks. Duodenum was collected at 48 h after the last bout of exercise. AMP-activated protein kinase (AMPK) α1 KD and wild-type mice were also utilized for investigating the mediatory role of AMPK on exercise-induced duodenal epithelial development. AMPK and peroxisome proliferator-activated receptor γ coactivator-1 α were upregulated by exercise via APJ activation in the intestinal duodenum. Correspondingly, exercise induced permissive histone modifications in the PR domain containing 16 (PRDM16) promoter to activate its expression, which was dependent on APJ activation. In agreement, exercise elevated the expression of mitochondrial oxidative markers. The expression of intestinal epithelial markers was downregulated due to AMPK deficiency, and AMPK signalling facilitated epithelial renewal. These data demonstrate that exercise-induced activation of the APJ-AMPK axis facilitates the homeostasis of the intestinal duodenal epithelium. KEY POINTS: Apelin receptor (APJ) signalling is required for improved epithelial homeostasis of the small intestine in response to exercise. Exercise intervention activates PRDM16 through inducing histone modifications, enhanced mitochondrial biogenesis and fatty acid metabolism in duodenum. The morphological development of duodenal villus and crypt is enhanced by the muscle-derived exerkine apelin through the APJ-AMP-activated protein kinase axis.

Metabolomic profiling for the preventive effects of dietary grape pomace against colorectal cancer.

Colorectal cancer (CRC) is one of the most common and deadly cancers worldwide. Grape pomace (GP) is a rich source of bioactive compounds with anti-inflammatory, and anticancer effects. We recently found that dietary GP had protective effects against CRC development in the azoxymethane (AOM)/dextran sulfate sodium (DSS) CRC mouse model through suppression of cell proliferation and modulation of DNA methylation. However, the underlying molecular mechanisms associated with changes in metabolites remain unexamined. This study profiled fecal metabolomic changes in a mouse CRC model in response to GP supplementation using gas chromatography-mass spectrometry (GC-MS) based metabolomic analysis. A total of 29 compounds showed significant changes due to GP supplementation, including bile acids, amino acids, fatty acids, phenols/flavonoids, glycerolipids, carbohydrates, organic acids, and others. The major changes in metabolites of feces include increased deoxycholic acid (DCA) and decreased amino acid content. Dietary GP upregulated the expression of farnesoid X receptor (FXR) downstream genes while decreasing fecal urease activity. DNA repair enzyme MutS Homolog 2 (MSH2) was upregulated by GP supplementation. Consistently, γ-H2AX, as a DNA damage marker, decreased in GP supplemented mice. Moreover, MDM2, a protein in the ataxia telangiectasia mutated (ATM) signaling, was decreased by GP supplementation. These data provided valuable metabolic clues for unraveling the protective effects of GP supplementation against CRC development.

Practice and Progress: Updates on Outbreaks, Advances in Research, and Processing Technologies for Low-moisture Food Safety.

Large, renowned outbreaks associated with low-moisture foods (LMFs) bring to light some of the potential, inherent risks that accompany foods with long shelf lives if pathogen contamination occurs. Subsequently, in 2013, Beuchat et al. (2013) noted the increased concern regarding these foods, specifically noting examples of persistence and resistance of pathogens in low-water activity foods (LWAFs), prevalence of pathogens in LWAF processing environments, and sources of and preventive measures for contamination of LWAFs. For the last decade, the body of knowledge related to LMF safety has exponentially expanded. This growing field and interest in LMF safety have led researchers to delve into survival and persistence studies, revealing that some foodborne pathogens can survive in LWAFs for months to years. Research has also uncovered many complications of working with foodborne pathogens in desiccated states, such as inoculation methods and molecular mechanisms that can impact pathogen survival and persistence. Moreover, outbreaks, recalls, and developments in LMF safety research have created a cascading feedback loop of pushing the field forward, which has also led to increased attention on how industry can improve LMF safety and raise safety standards. Scientists across academia, government agencies, and industry have partnered to develop and evaluate innovate thermal and nonthermal technologies to use on LMFs, which are described in the presented review. The objective of this review was to describe aspects of the extensive progress made by researchers and industry members in LMF safety, including lessons-learned about outbreaks and recalls, expansion of knowledge base about pathogens that contaminate LMFs, and mitigation strategies currently employed or in development to reduce food safety risks associated with LMFs.

Stage-specific nutritional management and developmental programming to optimize meat production.

Over the past few decades, genetic selection and refined nutritional management have extensively been used to increase the growth rate and lean meat production of livestock. However, the rapid growth rates of modern breeds are often accompanied by a reduction in intramuscular fat deposition and increased occurrences of muscle abnormalities, impairing meat quality and processing functionality. Early stages of animal development set the long-term growth trajectory of offspring. However, due to the seasonal reproductive cycles of ruminant livestock, gestational nutrient deficiencies caused by seasonal variations, frequent droughts, and unfavorable geological locations negatively affect fetal development and their subsequent production efficiency and meat quality. Therefore, enrolling livestock in nutritional intervention strategies during gestation is effective for improving the body composition and meat quality of the offspring at harvest. These crucial early developmental stages include embryonic, fetal, and postnatal stages, which have stage-specific effects on subsequent offspring development, body composition, and meat quality. This review summarizes contemporary research in the embryonic, fetal, and neonatal development, and the impacts of maternal nutrition on the early development and programming effects on the long-term growth performance of livestock. Understanding the developmental and metabolic characteristics of skeletal muscle, adipose, and fibrotic tissues will facilitate the development of stage-specific nutritional management strategies to optimize production efficiency and meat quality.

AMP-activated protein kinase inhibition in fibro-adipogenic progenitors impairs muscle regeneration and increases fibrosis.

BACKGROUND: Following muscle injury, fibro-adipogenic progenitors (FAPs) are rapidly activated and undergo apoptosis at the resolution stage, which is required for proper muscle regeneration. When excessive FAPs remain, it contributes to fibrotic and fatty infiltration, impairing muscle recovery. Mechanisms controlling FAP apoptosis remain poorly defined. We hypothesized that AMP-activated protein kinase (AMPK) in FAPs mediates their apoptosis during the muscle regeneration. METHODS: To test, AMPKα1fl/fl PDGFRαCre mice were used to knock out AMPKα1 in FAPs. Following AMPKα1 knockout, the mice were injected with phosphate-buffered saline or glycerol to induce muscle injury. Tibialis anterior muscle and FAPs were collected at 3, 7 and 14 days post-injury (dpi) for further analysis. RESULTS: We found that AMPKα1 deletion in FAPs enhanced p65 translocation to the nuclei by 110% (n = 3; P < 0.01). AMPKα1 knockout group had a higher gene expression of MMP-9 (matrix metalloproteinase-9) by 470% (n = 3; P < 0.05) and protein level by 39% (n = 3; P < 0.05). Loss of AMPKα1 up-regulated the active TGF-ß1 (transforming growth factor-ß1) levels by 21% (n = 3; P < 0.05). TGF-ß promoted apoptotic resistance, because AMPKα1-deficient group had 36% lower cleaved Caspase 3 (cCAS3) content (n = 3; P < 0.05). Fibrotic differentiation of FAPs was promoted, with increased collagen protein level by 54% (n = 3; P < 0.05). Moreover, obesity decreased phosphorylation of AMPK by 54% (n = 3; P < 0.05), which decreased cCAS3 in FAPs by 44% (n = 3; P < 0.05) and elevated collagen accumulation (52%; n = 3; P < 0.05) during muscle regeneration. CONCLUSIONS: These data suggest that AMPK is a key mediator of FAPs apoptosis, and its inhibition due to obesity results in fibrosis of regenerated muscle.

Listeria monocytogenes cross-contamination during apple waxing and subsequent survival under different storage conditions.

This study evaluated Listeria monocytogenes cross-contamination between inoculated fruits, waxing brush, and uninoculated fruits during apple wax coating and investigated the fate of L. monocytogenes on wax-coated apples introduced via different wax coating schemes. There were 1.8-1.9 log10 CFU/apple reductions of L. monocytogenes on PrimaFresh 360, PrimaFresh 606, or Shield-Brite AP-450 coated apples introduced before wax coating after 6 weeks of ambient storage (22 °C and ambient relative humidity). L. monocytogenes showed a similar trend (P > 0.05) on waxed apples under cold storage (1 °C and ∼ 90% relative humidity); there were 1.8-2.0 log10 CFU/apple reductions of L. monocytogenes during the 12 weeks of cold storage regardless of wax coating type. For cross-contamination study, a waxing brush was used to wax one inoculated apple (6.2 log10 CFU/apple); then, this brush was used to wax five uninoculated apples in a sequence. There were 3.7, 3.5, 3.3, 2.9, and 2.7 log10 CFU/apple and 3.6 log10 CFU/brush of L. monocytogenes transferred from the inoculated apple to uninoculated apple 1 to apple 5, and the waxing brush, respectively. The die-off rate of L. monocytogenes on wax-coated apples contaminated during wax coating was not significantly different from that contaminated on apples before wax coating, and 1.8-1.9 log10 CFU/apple reductions were observed during the 12 weeks of cold storage. The application of wax coatings, regardless of wax coating type, did not impact the survival of endogenous yeasts and molds on apples during ambient or cold storage. L. monocytogenes transferred onto waxing brushes during wax coating remained relatively stable during the 2-week ambient holding. Fungicide application during wax coating reduced (P < 0.05) yeast and mold counts but had a minor impact (P > 0.05) on the survival of L. monocytogenes on apples after 12 weeks of cold storage. Collectively, this study indicated that a high cross-contamination risk of L. monocytogenes during apple waxing, and L. monocytogenes on wax-coated apples introduced via different scenarios is stable during subsequent cold storage, highlighting the need for potential intervention strategies to control L. monocytogenes on wax-coated apples.

Prebiotic effects of goji berry in protection against inflammatory bowel disease.

The prevalence of inflammatory bowel disease (IBD) is increasing, which is concerning because IBD is a known risk factor for the development of colorectal cancer. Emerging evidence highlights environmental factors, particularly dietary factors and gut microbiota dysbiosis, as pivotal inducers of IBD onset. Goji berry, an ancient tonic food and a nutraceutical supplement, contains a range of phytochemicals such as polysaccharides, carotenoids, and polyphenols. Among these phytochemicals, L. barbarum polysaccharides (LBPs) are the most important functional constituents, which have protective effects against oxidative stress, inflammation, and neurodegeneration. Recently, the beneficial effects of goji berry and associated LBPs consumption were linked to prebiotic effects, which can prevent dysbiosis associated with IBD. This review assessed pertinent literature on the protective effects of goji berry against IBD focusing on the gut microbiota and their metabolites in mediating the observed beneficial effects.

Unraveling enterohemorrhagic Escherichia coli infection: the promising role of dietary compounds and probiotics in bacterial elimination and host innate immunity boosting.

The innate immune system has developed sophisticated strategies to defense against infections. Host cells utilize the recognition machineries such as toll-like receptors and nucleotide binding and oligomerization domain-like receptors to identify the pathogens and alert immune system. However, some pathogens have developed tactics to evade host defenses, including manipulation of host inflammatory response, interference with cell death pathway, and highjack of phagocytosis signaling for a better survival and colonization in host. Enterohemorrhagic Escherichia coli (EHEC) is a notorious foodborne pathogen that causes severe tissue damages and gastrointestinal diseases, which has been reported to disturb host immune responses. Diverse bioactive compounds such as flavonoids, phenolic acids, alkaloids, saccharides, and terpenoids derived from food varieties and probiotics have been discovered and investigated for their capability of combating bacterial infections. Some of them serve as novel antimicrobial agents and act as immune boosters that harness host immune system. In this review, we will discuss how EHEC, specifically E. coli O157:H7, hijacks the host immune system and interferes with host signaling pathway; and highlight the promising role of food-derived bioactive compounds and probiotics in harnessing host innate immunity and eliminating E. coli O157:H7 infection with multiple strategies.

Broccoli-Derived Glucoraphanin Activates AMPK/PGC1α/NRF2 Pathway and Ameliorates Dextran-Sulphate-Sodium-Induced Colitis in Mice.

As the prevalence of inflammatory bowel diseases (IBD) rises, the etiology of IBD draws increasing attention. Glucoraphanin (GRP), enriched in cruciferous vegetables, is a precursor of sulforaphane, known to have anti-inflammatory and antioxidative effects. We hypothesized that dietary GRP supplementation can prevent mitochondrial dysfunction and oxidative stress in an acute colitis mouse model induced by dextran sulfate sodium (DSS). Eight-week-old mice were fed a regular rodent diet either supplemented with or without GRP. After 4 weeks of dietary treatments, half of the mice within each dietary group were subjected to 2.5% DSS treatment to induce colitis. Dietary GRP decreased DSS-induced body weight loss, disease activity index, and colon shortening. Glucoraphanin supplementation protected the colonic histological structure, suppressed inflammatory cytokines, interleukin (IL)-1ß, IL-18, and tumor necrosis factor-α (TNF-α), and reduced macrophage infiltration in colonic tissues. Consistently, dietary GRP activated AMP-activated protein kinase (AMPK), peroxisome proliferator-activated receptor-gamma coactivator (PGC)-1α, and nuclear factor erythroid 2-related factor 2 (NRF2) pathways in the colonic tissues of DSS-treated mice, which was associated with increased mitochondrial DNA and decreased content of the oxidative product 8-hydroxydeoxyguanosine (8-OHDG), a nucleotide oxidative product of DNA. In conclusion, dietary GRP attenuated mitochondrial dysfunction, inflammatory response, and oxidative stress induced by DSS, suggesting that dietary GRP provides a dietary strategy to alleviate IBD symptoms.