Number Of Secretory Cells Research Articles

Oxidative stress, histopathological and genotoxicity of copper oxide nanoparticles in Biomphalaria alexandrina snail

AbstractHigher usage of copper oxide nanomaterials in industrial and biomedical fields may cause an increase of these nanoparticles in aquatic environments, which could have a detrimental ecological effect. Thus, the objective of this study was to evaluate the acute toxicity of copper oxide nanoparticles on the freshwater gastropod, Biomphalaria alexandrina. Transmission electron microscopy, x-ray diffraction analysis and UV–VIS spectrophotometer of CuO NPs revealed a typical TEM image and a single crystal structure with average crystallite size of approximately 40 nm also, a sharp absorption band was appeared. Following exposure to sub-lethal concentrations of CuO NPs (LC10, 15.6 mg/l and LC25, 27.2 mg/l), treated snails revealed a significant decrease (p < 0.05) in total antioxidant capacity, reduced glutathione contents as well as catalase, and sodium dismutase activities were significantly declined (p < 0.05) in comparison to the control group. Also, histopathological alterations were observed in the digestive gland, including ruptured and vacuolated digestive cells, and a marked increase in the number of secretory cells and the severity of the damage increased with rising concentrations. Furthermore, changes in RAPD profiles were detected in the treated snails. In conclusion, our research highlights the potential ecological impact of CuO NPs release in aquatic ecosystems and advocates for improved monitoring and regulation of CuO NPs industrial usage and disposal.

403 Impact of lysine, methionine, and histidine deficiencies on gene expression and upstream transcriptional regulators in bovine mammary epithelial cells: An RNA-sequencing analysis

Abstract Essential (E) amino acids (AA) may alter bovine mammary epithelial cell functions by impacting mRNA expression of genes through their upstream transcription factors. The objective of this research was to study the impact of EAA deficiencies on gene expression and to identify upstream transcriptional factors mediating their effects in bovine mammary epithelial cells. Epithelial cells were collected from the mammary glands of lactating dairy cows and cultured in combined media of DMEM/F12 and Medium 170, differentiated for 5 d, and subsequently treated in triplicate for 60 h with a control medium containing all EAA at normal plasma concentrations for cows (CTL), or a medium with 20 μM Lys (LY), 5 μM Met (LM), or 10 μM His (LH), which are each 25% of normal concentration. RNA was isolated from the cells and sequenced on an Illumina NovaSeq 6000 producing 150 base pair paired-end reads with a minimum sequencing depth of 150 million reads. Reads were cleaned with ‘fastp’ (Chen et al., 2018), aligned to the bovine reference genome (ARS-UCD1.2) using ‘STAR’ aligner (Dobin et al., 2013), and genes counted using ‘featureCounts’ (Liao et al., 2014). Differential expression of genes between treatment pairs was determined using the ‘DESeq2’ package (Love et al., 2014) in R. Genes with an absolute log2 fold change ≥ 1 and a false discovery rate of < 0.05 were considered differentially expressed. The number of differentially expressed genes relative to CTL was 780 for LY, 383 for LH, and 536 for LM. QIAGEN Ingenuity Pathway Analysis (IPA) identified four pathways consistently affected across LY, LM, and LH: kinetochore metaphase signaling, mitotic roles of polo-like kinase, cell cycle: G2/M DNA damage checkpoint regulation, and interferon signaling (Figure 1-3). Notably, the kinetochore metaphase signaling pathway was identified as the most significant across all treatments, suggesting a strong link to cell proliferation and apoptosis during EAA deficiency. The interferon signaling might be related to the Janus kinase 2/signal transducer and activator of transcription 5 (Jak2/STAT5) pathway which can promote the expression of genes encoding milk proteins such as β-casein and β-lactoglobulin. Furthermore, the IPA identified upstream transcription factors related to cell proliferation, apoptosis, autophagy, protein translation, endoplasmic reticulum biogenesis, and amino acid metabolism including NUPR1, FOXM1, MYC, CCND1, TP53, DDIT3, and ATF4 across all treatments. The findings suggest that AA deprivation regulates bovine mammary epithelial cell function by instigating amino acid response pathways and altering secretory cell number.

High-grade serous ovarian cancer (HGSOC) with fallopian tube involvement.

Literature data present new studies about precancerous lesions of pelvic serous carcinoma that originate from the tubal secretory cells. It has long been thought that ovarian cancer cannot be prevented by prophylactic screening or surgery. In recent years, gynecologists have adapted to new principles and so, during routine hysterectomies in perimenopausal women for benign uterine pathologies, salpingo-oophorectomy is performed as a prophylactic approach. The purpose of our article was to draw attention to the association between abnormal fallopian tube pathology and the presence of serous ovarian neoplasia in perimenopausal women at risk. We report the case of a 45-year-old woman who had unspecific symptoms of abdominal pain and loss of appetite and weight. A pelvic magnetic resonance imaging was performed, and an ovarian mass was detected. Our case shows that the fallopian tube can be the primary point of origin for a pelvic disease, therefore prevention is possible with early computed tomography scan and annual ultrasound. The patient presented with a T1c staging post-surgery and her chances of survival could have decreased if she had postponed medical examination longer. We found a significant increase in the absolute number of tubal secretory cells in patients with ovarian neoplasia, which supports the assumption that serous tubal intraepithelial carcinoma lesions are found especially in the serous ovarian type. Our article is a strong suggestion that serous ovarian cancer originates from the fallopian tube and can potentially serve as a sensitive biomarker for early serous carcinogenesis within the fallopian tube.

Impact of Zinc Oxide on the Development of Aspergillus-Induced Maxillary Sinusitis Rabbit Model.

Aspergillus fumigatus is commonly found in the airway and is associated with airway inflammatory diseases. Zinc oxide (ZO) is known to be an essential microelement that facilitates fungal survival, growth, and proliferation. This study aimed to investigate the impact of ZO on A. fumigatus-induced fungal sinusitis in rabbits. Twenty-eight New Zealand white rabbits were divided into four groups for this study. Group 1 (6 sides) was treated with intramaxillary phosphate buffer saline (PBS) served as the negative control, Group 2 (6 sides) received intramaxillary PBS and ZO, Group 3 (8 sides) was treated with intramaxillary A. fumigatus alone, and Group 4 (8 sides) treated with intramaxillary A. fumigatus with ZO. After 4 and 12 weeks, sinus mucosal cytokine and transcription factor expressions were determined. A histological analysis was performed to determine inflammatory cell infiltration, number of secretory cells, and mucosal thickness. Fungal biofilm formation was determined using confocal laser microscopy. The intramaxillary instillation of A. fumigatus conidia led to an increase in protein and mRNA expression of interleukin (IL)-1β and IL-8 in the maxillary sinus mucosa. They were associated with mitogen-activated protein kinase and activator protein-1. Furthermore, intramaxillary instillation of fungal conidia resulted in significant enhancement of inflammatory cell infiltration, epithelial thickening, and fungal biofilm formation. However, intramaxillary ZO did not have a significant impact on A. fumigatus-induced cytokine protein and mRNA expression, and inflammatory cell infiltration and epithelial thickness in sinonasal mucosa. While intramaxillary instillation of A. fumigatus increased mucosal inflammation, cytokine production, and biofilm formation, the intramaxillary application of ZO did not have a significant influence on inflammation in the maxillary sinus mucosa.

Erbb3 regulation of secretory differentiation in the intestinal epithelium

Background: Previous work by our lab showed that intestinal-specific deletion of the ErbB3 receptor tyrosine kinase results in increased ileal Paneth cell numbers. These cells produce host defense peptides and support stem cells with growth factors. The mechanisms by which ErbB3 regulates Paneth cells are not well understood, but a candidate mediator is the polycomb repressor complex 1 component BMI1, which marks secretory progenitor cells. Furthermore, while there are no Paneth cells in the mouse colon, deep crypt secretory (DCS) cells are a distinct Reg4+ population that have some functional overlap with both Paneth and goblet cells; we will also test whether ErbB3 regulates DCS differentiation. Overall we are testing the hypothesis that ErbB3 regulates secretory cell numbers through BMI1. Methods: We bred Villin-Cre;ErbB3flox/flox mice (ErbB3ΔIE) to delete ErbB3 from the intestinal epithelium. Colonic sections from ErbB3ΔIE and ErbB3flox/flox littermates were subjected to RNAscope in situ hybridization for Reg4. RNA from mucosal scrapings (both ileum and colon) was assessed by qPCR for Reg4, Bmi1, and Lgr5. To test signaling mechanisms, we treated HT-29 cells with NRG-1β to activate ErbB3, +/- inhibitors to PI3K (LY294002), MEK/MAPK (U0126), or BMI1 (PTC-209). Colonoids and enteroids from ErbB3ΔIE and ErbB3flox/flox mice were used to confirm responses in a non-transformed system. Results: In ErbB3ΔIE mice, the colonic epithelium showed increased Reg4 levels and more Reg4+ cells compared to littermate controls, similar to our published data for the Paneth cell marker Lyz1 in ileum. BMI1 RNA and protein levels were also increased in both small and large intestinal mucosal scrapings from ErbB3ΔIE mice vs. littermates. ErbB3ΔIE colonoids had increased Reg4 versus control colonoids, and NRG-1β reduced levels in control but not ErbB3ΔIE cultures. Ileal enteroids showed a decrease in Lyz1 expression with Bmi1 inhibition and an increase in Bmi1 expression with PI3K and MAPK blockade. In HT-29 cells, NRG-1β treatment reduced Reg4 and Bmi1 expression. Conversely, Reg4 and Bmi1 were induced by PI3K inhibition with LY294002 (p<0.03) (p<0.0005) or MEK/MAPK inhibition with U0126 (p<0.05) (p<0.0001). Conclusions: NRG1-ErbB3 signaling restricts both ileal Paneth ( Lyz1+) and colonic DCS ( Reg4+) cell numbers. Furthermore, ErbB3 regulates Bmi1 expression through PI3K/Akt and MAPK signaling and BMI1 activity promotes secretory cell development. Since loss of DCS or Paneth cells has been shown to disrupt the intestinal stem cell niche and secretory cell markers are altered in several intestinal disease states, these results may point to potential future therapeutic avenues targeting this regulatory mechanism. NIH/NIDDK award R01DK095004. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Characterization of age-associated gene expression changes in mouse sweat glands.

Evaporation of sweat on the skin surface is the major mechanism for dissipating heat in humans. The secretory capacity of sweat glands (SWGs) declines during aging, leading to heat intolerance in the elderly, but the mechanisms responsible for this decline are poorly understood. We investigated the molecular changes accompanying SWG aging in mice, where sweat tests confirmed a significant reduction of active SWGs in old mice relative to young mice. We first identified SWG-enriched mRNAs by comparing the skin transcriptome of Eda mutant Tabby male mice, which lack SWGs, with that of wild-type control mice by RNA-sequencing analysis. This comparison revealed 171 mRNAs enriched in SWGs, including 47 mRNAs encoding 'core secretory' proteins such as transcription factors, ion channels, ion transporters, and trans-synaptic signaling proteins. Among these, 28 SWG-enriched mRNAs showed significantly altered abundance in the aged male footpad skin, and 11 of them, including Foxa1, Best2, Chrm3, and Foxc1 mRNAs, were found in the 'core secretory' category. Consistent with the changes in mRNA expression levels, immunohistology revealed that higher numbers of secretory cells from old SWGs express the transcription factor FOXC1, the protein product of Foxc1 mRNA. In sum, our study identified mRNAs enriched in SWGs, including those that encode core secretory proteins, and altered abundance of these mRNAs and proteins with aging in mouse SWGs.

Early Atf4 activity drives airway club and goblet cell differentiation.

Activating transcription factor 4 (Atf4), which is modulated by the protein kinase RNA-like ER kinase (PERK), is a stress-induced transcription factor responsible for controlling the expression of a wide range of adaptive genes, enabling cells to withstand stressful conditions. However, the impact of the Atf4 signaling pathway on airway regeneration remains poorly understood. In this study, we used mouse airway epithelial cell culture models to investigate the role of PERK/Atf4 in respiratory tract differentiation. Through pharmacological inhibition and silencing of ATF4, we uncovered the crucial involvement of PERK/Atf4 in the differentiation of basal stem cells, leading to a reduction in the number of secretory cells. ChIP-seq analysis revealed direct binding of ATF4 to regulatory elements of genes associated with osteoblast differentiation and secretory cell function. Our findings provide valuable insights into the role of ATF4 in airway epithelial differentiation and its potential involvement in innate immune responses and cellular adaptation to stress.

The mechanism of intestinal stem cells differentiation after ischemia-reperfusion injury in a rat model.

Notch and Wnt/β-catenin signaling are responsible for regulation of intestinal stem cells (ISCs) proliferation and differentiation. The purpose of the study was to evaluate Wnt/β-catenin and Notch signaling roles in regulation of ISC differentiation following ischemia-reperfusion (IR) injury in a rat. Rats were assigned into two groups: Sham rats underwent laparotomy without vascular intervention and IR rats underwent occlusion of SMA and portal vein for 20min followed by 48h of reperfusion. Wnt/β-catenin and Notch-related gene expression were determined using Real-Time PCR. Enterocyte proliferation, differentiation and Wnt-related proteins were determined by immunohistochemistry. IR rats demonstrated a significant decrease in β-catenin gene expression, a decrease in cyclin D1 and β-catenin positive cells in jejunum and ileum compared to Sham rats. IR rats demonstrated a significant increase in Notch-related gene expression in jejunum and ileum compared to Sham rats. The number of secretory cells was higher mainly in the jejunum and number of absorptive cells was significantly lower in jejunum and lower in ileum in IR rats compared to Sham rats. Intestinal stem-cell differentiation is toward secretory cells 48h after IR injury; however, Wnt/β-catenin pathway inhibition and Notch-related gene expression stimulation suggest crosstalk between pathways.

Linderae Radix water extract treats diarrhea-predominant irritable bowel syndrome in rats: a serum metabolomics study

This study aims to investigate the mechanism of Linderae Radix water extract(LRWE) in the prevention and treatment of diarrhea-predominant irritable bowel syndrome(IBS-D) based on serum metabolomics. Eighteen 2-week-old male SD rats were randomized into control, IBS-D model, and LRWE groups. The rats in other groups except the control group received gavage of senna concentrate combined with restraint stress for the modeling of IBS-D. The rats in the LRWE group were administrated with LRWE(5.4 g·kg~(-1)) by gavage, and those in the control and IBS-D model groups with an equal volume of distilled water for a total of 14 days. The visceral sensitivity was evaluated by the abdominal withdrawal reflex(AWR) score, and the degree of diarrhea was assessed by the fecal water content(FWC). The morphological changes of the colon and the morphology and number of goblet cells were observed by hematoxylin-eosin(HE) and periodic acid-schiff(PAS) staining, respectively. Ultra-high performance liquid chromatography-tandem mass spectrometry(UPLC-MS/MS) was used for the screening of the potential biomarkers in the rat serum and their related metabolic pathways. The results showed that LRWE reduced the AWR score, decreased FWC, and alleviated visceral sensitivity and diarrhea symptoms in IBS-D rats. HE and PAS staining showed that LRWE mitigated low-grade intestinal inflammation and increased the number of mature secretory goblet cells in the colonic epithelium of IBS-D rats. A total of 25 potential biomarkers of LRWE in treating IBS-D were screened out in this study, which were mainly involved in riboflavin, tryptophan, glycine, serine and threonine metabolism, glyoxylate and dicarboxylate metabolism, and cysteine and methionine metabolism. The regulatory effects were the most significant on the riboflavin and tryptophan metabolism pathways. LRWE may alleviate the visceral hypersensitivity by promoting energy metabolism and amino acid metabolism, enhancing intestinal barrier function, and improving intestinal immune function in IBS-D rats.

Three-dimensional cultured ampullae from rats as a screening tool for vestibulotoxicity: Proof of concept using styrene

Numerous ototoxic drugs, such as some antibiotics and chemotherapeutics, are both cochleotoxic and vestibulotoxic (causing hearing loss and vestibular disorders). However, the impact of some industrial cochleotoxic compounds on the vestibular receptor, if any, remains unknown. As in vivo studies are long and expensive, there is considerable need for predictive and cost-effective in vitro models to test ototoxicity. Here, we present an organotypic model of cultured ampullae harvested from rat neonates. When cultured in a gelatinous matrix, ampulla explants form an enclosed compartment that progressively fills with a high-potassium (K+) endolymph-like fluid. Morphological analyses confirmed the presence of a number of cell types, sensory epithelium, secretory cells, and canalar cells. Treatments with inhibitors of potassium transporters demonstrated that the potassium homeostasis mechanisms were functional. To assess the potential of this model to reveal the toxic effects of chemicals, explants were exposed for either 2 or 72 h to styrene at a range of concentrations (0.5–1 mM). In the 2-h exposure condition, K+ concentration was significantly reduced, but ATP levels remained stable, and no histological damage was visible. After 72 h exposure, variations in K+ concentration were associated with histological damage and decreased ATP levels. This in vitro 3D neonatal rat ampulla model therefore represents a reliable and rapid means to assess the toxic properties of industrial compounds on this vestibular tissue, and can be used to investigate the specific underlying mechanisms.

A mouse model and pathogenesis study for CVA19 first isolated from hand, foot, and mouth disease

ABSTRACT Coxsackievirus A19 (CVA19) is a member of Enterovirus (EV) C group in the Picornaviridae family. Recently, we reported a case of CVA19-infected hand, foot, and mouth disease (HFMD) for the first time. However, the current body of knowledge on the CVA19 infection, particularly the pathogenesis of encephalomyelitis and diarrhoea is still very limited, due to the lack of suitable animal models. Here, we successfully established a CVA19 mouse model via oral route based on 7-day-old ICR mice. Our results found the virus strain could directly infect the neurons, astrocytes of brain, and motor neurons of spinal cord causing neurological complications, such as acute flaccid paralysis. Importantly, viruses isolated from the spinal cords of infected mice caused severe illness in suckling mice, fulfilling Koch’s postulates to some extent. CVA19 infection led to diarrhoea with typical pathological features of shortened intestinal villi, increased number of secretory cells and apoptotic intestinal cells, and inflammatory cell infiltration. Much higher concentrations of serum cytokines and more peripheral blood inflammatory cells in CVA19-infected mice indicated a systematic inflammatory response induced by CVA19 infection. Finally, we found ribavirin and CVA19 VP1 monoclonal antibody could not prevent the disease progression, but higher concentrations of antisera and interferon alpha 2 (IFN-α2) could provide protective effects against CVA19. In conclusion, this study shows that a natural mouse-adapted CVA19 strain leads to diarrhoea and encephalomyelitis in a mouse model via oral infection, which provides a useful tool for studying CVA19 pathogenesis and evaluating the efficacy of vaccines and antivirals.

Mechanism underlying the modulation of milk production by incomplete milking.

Mammary gland secretory activity is modulated by systemic and local factors; however, the relationship between these factors is unknown. The aim of this study was to determine how a local factor, such as incomplete milking, affects mammary epithelial cell activity, number, and responsiveness to blood prolactin (PRL). Eight cows in mid-lactation were differentially milked (i.e., their right quarters were milked incompletely at approximately 70%, and their left quarters were milked completely, twice daily for 4 wk). Throughout the experiment, milk yield was measured at the quarter level. Milk samples were collected from each quarter once a week to assess the milk components, and epithelial cell concentrations, as well as to isolate milk fat globule RNA. In the weeks before and after the experiment, mammary gland functional capacity was evaluated by measuring the volume of milk harvested after complete filling of the gland. At the end of the last experimental week, mammary gland biopsies were performed on each rear quarter. The milk production of quarters milked completely remained stable during the treatment period, whereas, as expected, the milk production of quarters milked incompletely was only 53% of completely milked quarters at the end of the period. Accordingly, the expression of genes related to milk synthesis (CSN2, LALBA, and ACACA) in milk fat was lower in the quarters that were milked incompletely. Incomplete milking decreased the milk lactose content, indicating a loss of integrity of tight junctions. The total yield of epithelial cells in milk was not affected, but their concentration in milk, the BAX:BCL2 gene expression ratio, and the loss of mammary functional capacity were greater in the quarters milked incompletely, suggesting an acceleration of involution in those quarters. The expression of the short isoform of the PRL receptor gene (PRLR) tended to be lower, and the expression of STAT5A and STAT5B tended to decline in the quarters milked incompletely. In mammary gland biopsy samples, the number of both short and long isoforms of the PRLR were not affected, nor were the amount and activation of STAT3 and STAT5. However, the ratio of PRLR short isoform to PRLR long isoform was lower in the quarters milked incompletely. The decrease in milk yield induced by incomplete milking is rapid and associated with a decrease in mammary epithelial cell activity and a decrease in the number of secretory epithelial cells. The results of this experiment provide only limited support for the hypothesis that modulation of the mammary gland's responsiveness to PRL is part of the mechanism by which local factors, such as incomplete milking, modulate milk synthesis.

Deep Crypt Secretory Cell Differentiation in the Colonic Epithelium Is Regulated by Sprouty2 and Interleukin 13

Deep crypt secretory (DCS) cells are a critical component of the colonic stem cell niche. However, the regulatory mechanisms controlling DCS cell numbers and function are not well understood. Sprouty2 is an inflammation-responsive regulator of intracellular signaling that influences colonic secretory cell numbers in colitis via an epithelial-stromal interleukin (IL)33/IL13 signaling loop. Here, we tested the hypothesis that IL13, induced by epithelial Sprouty2 down-regulation, promotes DCS cell differentiation and function. Distal colons from mice with an intestinal epithelial-specific Sprouty2 deletion (Spry2ΔIE) and littermate controls were analyzed by in situ hybridization for Reg4+ DCS cells. Single-cell RNA sequencing and immunostaining were used to identify DCS cell-derived host defense peptides (HDPs) and localization of IL13 and IL13 receptor; bulk RNA sequencing and quantitative polymerase chain reaction were used to quantify changes in expression of identified HDPs. Cytokine-treated colonoids were assessed for DCS cells. A requirement for an IL33/IL13 signaling loop in the regulation of DCS cells was assessed invivo using IL13 null mice. Reg4+ DCS cell numbers were increased 2-fold in distal colons of Spry2ΔIE mice with a concomitant overall increase in DCS cell marker expression (Reg4, Spink4, and Agr2). Single-cell transcriptomics showed the HDP Retnlb/Resistin Like Beta (RELMβ) is highly enriched in DCS cells. Retnlb/RELMβ expression was increased in Spry2ΔIE colons. IL13, but not IL33, induced Reg4 and Retnlb expression in colonic epithelial organoids, and IL33-mediated expansion of the DCS cell population invivo was dependent on IL13, which was expressed predominantly by type II innate lymphoid cells in the colonic mucosa. Sprouty2 limits colonic DCS cell differentiation through suppression of IL13 signaling. At homeostasis, DCS cells are marked by high levels of the HDP RELMβ. Loss of epithelial Sprouty2 activates type II innate lymphoid cells to release IL13, promoting expansion of the DCS cell population and increased colonic RELMβ levels.

Schizochytrium limacinum altered antioxidant capacity and transcriptome profiles in Pacific white shrimp fed a low-fishmeal diet

Dietary low-fishmeal (FM) have negative impacts on growth performance and metabolic responses in aquatic animals, while Schizochytrium limacinum have multiple benefits due to its rich contents of docosahexaenoic acid (DHA). However, little information is available on the effects of S. limacinum on Pacific white shrimp (Litopenaeus vannamei) in a low-FM diet (LF). An 8-week feeding trial were used to investigate the impacts of S. limacinum on growth performance, as well as morphological changes, biochemical indicators, antioxidant capacity, and transcriptomic profiles of hepatopancreas in shrimp fed a low-FM diet. Compared to LF diet, 0.3% S. limacinum (LFLD) diet significantly decreased the specific growth rate (SGR), and did not affect the feed conversion rate (FCR) and weight gain rate (WGR); whereas 0.6% S. limacinum (LFHD) diet did not affect the SGR, FCR and WGR. Histological structures of hepatopancreas showed that LFLD and LFHD treatments reduced the number and size of secretory cells and increased the number of storage cells, compared to LF group. LFLD and LFHD diets significantly decreased the concentrations of triglyceride and total cholesterol, significantly increased the levels of glutathione peroxidase and total antioxidative capacity, while did not affect the levels of malondialdehyde and superoxide dismutase. A total of 135 differential expression genes (DEGs) were identified in LFLD group and 108 DEGs were identified in LFHD group (both compared to LF group). Administration of S. limacinum altered the transcriptomic profiles, while LFHD induced a pattern similar to that of LF. LFLD and LFHD treatments mainly affected the 9 KEGG metabolic pathways, including “Arachidonic acid metabolism” and “Glutathione metabolism”. In conclusion, LFLD treatment impaired the growth performance of shrimp, while LFHD treatment did not affect it; and both treatments improved the morphological structure, lipid accumulation and antioxidant capacity of hepatopancreas.

Bacillus subtilis programs the differentiation of intestinal secretory lineages to inhibit Salmonella infection.

The role of intestinal microbiota on fate determination of intestinal epithelial cells has not been extensively examined. In this study, we explore the effect of Bacillus subtilis on programmed intestinal epithelial differentiation. We find that B.subtilis stimulates the differentiation of intestinal secretory cells. Moreover, B.subtilis inhibits the Notch pathway to reduce the expression of hairy and enhancer of split 1, thereby shifting intestinal stem cell differentiation toward a secretory cell fate. Moreover, we demonstrate that the programming effect of B.subtilis on intestinal differentiation is Toll-like receptor 2 pathway dependent. B.subtilis is associated with increased numbers of Paneth and goblet cells in the intestine. This results in the production of antimicrobial peptides to protect the intestinal mucosal barrier against Salmonella typhimurium. This study demonstrates that B.subtilis contributes to the differentiation of secretory cells by affecting Notch pathway signaling to maintain the intestinal barrier.

Transcription Factor RrANT1 of Rosa rugosa Positively Regulates Flower Organ Size in Petunia hybrida.

The flower is the main organ that produces essential oils in many plants. The yield of raw flowers and the number of secretory epidermal cells are the main factors for essential oil production. The cultivated rose species “Pingyin 1” in China was used to study the effect of RrANT1 on floral organ development. Eighteen AP2 transcription factors with dual AP2 domains were identified from Rosa rugosa genome. RrANT1 belonged to euANT. The subcellular localization results showed that RrANT1 protein is localized in the nucleus. The relative expression level of RrANT1 in the receptacle is higher than that in petals in the developmental stages, and both decreased from the initial phase to senescence. Compared with the RrANT1 expression level in petals in the blooming stage, RrANT1 expression level was significant in petals (~48.8) and highest in the receptacle (~102.5) in the large bud stage. It was only highly expressed in the receptacle (~39.4) in the blooming period. RrANT1 overexpression significantly increased petunia flower and leaf sizes (~1.2), as well as flower fresh weight (~30%). The total number of epidermis cells in the petals of overexpressing plants significantly increased (>40%). This study concluded that RrANT1 overexpression can increase the size and weight of flowers by promoting cell proliferation, providing a basis for creating new rose germplasm to increase rose and essential oil yield.

Mentha pulegium L.: A Plant Underestimated for Its Toxicity to Be Recovered from the Perspective of the Circular Economy.

The aim of the study was to investigate the micromorphology of Mentha pulegium leaves and flowers harvested in three different Sicilian (Italy) areas with peculiar pedo-climatic conditions, and to characterize the phytochemical profile, the phytotoxic activity, and the eco-compatibility of their essential oils (EOs) for potential use as safe bioherbicides. Light microscopy (LM) and scanning electron microscopy (SEM) highlighted that M. pulegium indumentum consists of non-glandular and glandular trichomes of different types. Peltate trichomes of plants from the different sites showed few significant differences in dimension and abundance, but they were characterized by a surprisingly high number of secretory cells both in leaves and flowers. Phytochemical analyses showed that oxygenated monoterpenes were the most abundant class in all the EOs investigated (92.2–97.7%), but two different chemotypes, pulegone/isomenthone and piperitone/isomenthone, were found. The complex of morphological and phytochemical data indicates that soil salinity strongly affects the expression of the toxic metabolite pulegone, rather than the EO yield. Phytotoxicity tests showed a moderate activity of EOs against the selected species as confirmed by α-amylase assay. Moreover, the low toxicity on brine shrimp provided a rationale for the possible use of investigated EOs as eco-friendly herbicides.

Effect of Listeria monocytogenes on intestinal stem cells in the co-culture model of small intestinal organoids

Listeria monocytogenes is a foodborne pathogen that causes systemic infections by crossing the intestinal barrier. However, in vitro analysis of the interaction of L. monocytogenes and small intestinal epithelium has yet to be fully elucidated. To study host responses from intestinal epithelium during L. monocytogenes infection, we used the co-culture model of small intestinal organoids and L. monocytogenes. Results showed that L. monocytogenes mediated damage to intestinal epithelium, especially intestinal stem cells. L. monocytogenes was found to reduce budding rate and increase mortality of organoids. Moreover, it affected the proliferation of epithelial cells and numbers of secretory cells. In addition, it was demonstrated that L. monocytogenes stimulated a reduction in the number of Lgr5+ stem cells. Furthermore, L. monocytogenes affected the expression of Hes1, Math1 and Sox9 to interfere with the differentiation of intestinal stem cells. Collectively, our findings reveal the effects of L. monocytogenes infection on intestinal stem cells and demonstrate that small intestinal organoid is a suitable experimental model for studying intestinal epithelium–pathogen interactions.

A dynamic mammary gland model describing colostrum immunoglobulin transfer and milk production in lactating sows.

The physiology of the sow mammary gland is qualitatively well described and understood. However, the quantitative effect of various biological mechanisms contributing to the synthesis of colostrum and milk is lacking and more complicated to obtain. The objective of this study was to integrate physiological and empirical knowledge of the production of colostrum and milk in a dynamic model of a single sow mammary gland to understand and quantify parameters controlling mammary gland output. In 1983, Heather Neal and John Thornley published a model of the mammary gland in cattle, which was used as a starting point for the development of this model. The original cattle model was reparameterized, modified, and extended to describe the production of milk by the sow mammary gland during lactation and the prepartum production of colostrum as the combined output of immunoglobulins (Ig) and milk. Initially, the model was reparameterized to simulate milk synthesis potential of a single gland by considering biological characteristics and empirical estimations of sows and piglets. Secondly, the model was modified to simulate more accurately the responses to changes in milk removal rates. This was done by linking the ejectable milk storage capacity to the number of secretory cells rather than being constant throughout lactation. Finally, the model was extended to include the prepartum synthesis of milk and the kinetics of Ig into and out of the mammary gland. A progressive capacity of secretory cells to synthesize milk was used to differentiate the time between the onset of milk synthesis and Ig transfer. Changes in maximum milk removal rate, duration of milk ejection, and nursing interval exerted a great impact on the modeled milk output. Changes by ±60% in one of these parameters were capable of increasing milk output by 28% to 39% during the first 4 wk in lactation compared with the reference parameterization. This suggests that the ability of the piglet to remove milk from the gland exerts a key control on milk synthesis during lactation. Modeling colostrum as the combined output of Ig and milk allowed to represent the rapid decline in Ig concentration observed during the first hours after farrowing. In conclusion, biological and empirical knowledge was integrated into a model of the sow mammary gland and constitutes a simple approach to explore in which conditions and to what extent individual parameters influence Ig kinetics and milk production.

Single-Blinded Study Highlighting the Differences between the Small Intestines of Neonatal and Weaned Piglets.

Simple SummaryThe gut mucosa of pigs, which contains intestinal epithelium and subepithelial immune cells, forms a barrier against microorganisms. Nonetheless, infectious diseases of the digestive tract remain the most frequent and recurrent conditions in the swine industry. Changes in intestinal morphology and structure primarily occur at birth and during weaning. However, the difference in the intestinal structures between neonatal and weaned piglets remains unclear. In this study, for the first time, we evaluated the differences in the small intestine between neonatal (0-day-old) and weaned piglets (21-day-old) and analyzed the morphology and immunological components of the small intestines of 0- and 21-day-old piglets, thereby providing preliminary data for future mechanistic studies.The gut is one of the body’s major immune structures, and the gut mucosa, which contains intestinal epithelium and subepithelial immune cells, is the primary site for eliciting local immune responses to foreign antigens. Intestinal immune system development in pigs is a transitional period during birth and weaning. This study compares the morphological and immunological differences in the small intestine of neonatal and weaned piglets to potentially prevent intestinal infectious diseases in neonatal piglets. Histological analyses of weaned piglet intestines showed increased crypt depth, higher IEL count, and larger ileal Peyer’s patches compared with those of neonates. Additionally, the ileal villi of weaned piglets were longer than those of neonatal piglets, and claudin-3 protein expression was significantly higher in weaned than in neonatal piglets. The numbers of CD3+ T, goblet, and secretory cells were also higher in the small intestines of weaned piglets than in those of neonates. No significant differences were observed in the secretory IgA-positive cell number in the jejunum of weaned and neonatal piglets. The mRNA expression of most pattern recognition receptors genes in the duodenum and jejunum was higher in the weaned than neonatal piglets; however, the opposite was true in the ileum. The mRNA levels of IL-1β and TNF-α in the jejunal and ileal mucosa were higher in weaned piglets than in neonatal piglets. There were significantly fewer CD3+, CD4+, and CD8+ T cells from peripheral blood-mononuclear cells in neonatal piglets. Our study provides insights regarding the different immune mechanisms within the small intestines of 0- and 21-day-old piglets. Studies on the additional developmental stages and how differences in the small intestines affect the response of pigs to pathogens remain warranted.