Insect and Pesticide Research (8)Insect and Arachnid Ecology and Behavior (6)Plant and animal studies (5)Bee Products Chemical Analysis (4)GABA and Rice Research (4)
Frontiers in cellular and infection microbiology •
Alpha-galactosides (oligosaccharides) in nectar and pollen cause honey bee larval rot and worker bloats. Honey bee colonies surviving in forests for a long period have low rates of larval rot and worker bloats; however, the mechanism of oligosaccharide metabolism is unclear. In this study, we used metagenomics and metabolomics to investigate the structure and function of the gut flora and the digestion characteristics of oligosaccharides in the gut of foragers (CN group) that had been in the forest for a long period (continuously for 14 years), and those that had not been pollinated with (N group) after 24 h of consumption of honey. The results revealed that the abundance of up to 24.08%, which can metabolize α-galactoside (α-Gal), was significantly higher ( < 0.05) in the gut of foragers in the CN group than in the N group. Additionally, the gut flora of foragers in the CN group carried a significantly higher ( < 0.05) abundance of genes encoding α-galactosidase (Glycoside hydrolase family 4, GH4) than the N group. Similarly, metabolomic results indicated that the three toxic oligosaccharides in honey were lower in the gut of CN group foragers. These results suggest that the gut flora of , which inhabits oil tea forests for long periods of time, changes and adapts to the predominant ecological niche, enhancing the host's ability to metabolize toxic oligosaccharides. This important discovery provides positive guidance for the subsequent directions for breeding of ( enrichment and GH4 upregulation), specialized in pollinating .
Li Z, Ma A, Miller I, Starnes R, Talkington A, et al.
Journal of controlled release : official journal of the Controlled Release Society •
Polyethylene glycol (PEG) is frequently used in various protein and nanomedicine therapeutics. However, various studies have shown that select PEGylated therapeutics can induce production of anti-PEG antibodies (APA), potentially culminating in rapid clearance from the systemic circulation, loss of efficacy and possibly increased risks of allergic reactions. Although IgE is a frequent cause of immediate hypersensitivity reactions (IHR), the role of IgE APA in PEG-related IHR is not well understood, due in part to a lack of standardized assays for measuring IgE APA. Here, we developed a rigorous competitive ELISA method to measure the concentrations of various APA isotypes, including IgE, with picomolar sensitivities. In a small number of serum samples from patients with known PEG allergy, the assay allowed us to detect a strong correlation between IgG and IgE APA in individuals with history of allergic reactions to PEG or PEGylated drugs, but not between IgM and IgE APA. We detected appreciable levels of IgG and IgM APA in individuals with history of alpha-gal allergy, however, they were not elevated relative to those detected in other healthy controls, and we found no pre-existing IgE APA. While preliminary and should be further investigated, these results suggest that differences in the route and mechanism of PEG exposure may drive variability in APA response.
Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine] •
To investigate the role of inflammatory biomarkers in the relationship between blood lead levels and blood pressure changes. A total of 9 910 people aged 18-79 years who participated in the China National Human Biomonitoring in 2017-2018 were included in this study. A self-made questionnaire was used to collect demographic characteristics, lifestyle and other information, and the data including height, weight and blood pressure were determined through physical examination. Blood and urinary samples were collected for the detection of blood lead and cadmium levels, urinary arsenic levels, white blood cells, neutrophils, lymphocytes, and hypersensitive C-reactive protein (hs-CRP). Weighted linear regression models were used to evaluate the associations between blood lead, inflammatory biomarkers and blood pressure. Mediation analysis was performed to investigate the role of inflammation in the relationship between blood lead levels and blood pressure changes. The median (, ) age of all participants was 45.4 (33.8, 58.4)years, including 4 984 males accounting for 50.3%. Multivariate logistic regression model analysis showed that after adjusting for age, gender, residence area, BMI, education level, smoking and drinking status, family history of hypertension, consumption frequency of rice, vegetables, and red meat, fasting blood glucose, total cholesterol, triglycerides, blood cadmium and urinary arsenic levels, there was a positive association between blood lead levels, inflammatory biomarkers and blood pressure (<0.05). Each 2.71 μg/L (log-transformed) increase of the lead was associated with a 2.05 (95%: 0.58, 3.53) mmHg elevation in systolic blood pressure (SBP), 2.24 (95%: 1.34, 3.14) mmHg elevation in diastolic blood pressure (DBP), 0.25 (95%: 0.05, 0.46) mg/L elevation in hs-CRP, 0.16 (95%: 0.03, 0.29)×10/L elevation in white blood cells, and 0.11 (95%: 0.02, 0.21)×10/L elevation in lymphocytes, respectively. Mediation analysis showed that the levels of hs-CRP significantly mediated the association of blood lead with SBP, with a proportion about 3.88% (95%: 0.45%, 7.32%). The analysis also found that the levels of hs-CRP and neutrophils significantly mediated the association of blood lead with SBP, with a proportion about 4.10% (95%: 1.11%, 7.10%) and 2.42% (95%: 0.07%, 4.76%), respectively. This study suggests that inflammatory biomarkers could significantly mediate the association of blood lead levels and blood pressure changes.
Obesity has become a common health concern around the world. Maternal obesity could cause poor reproductive outcomes due to chronic ovarian inflammation and decreased oocyte quality. However, the strategies to improve the poor reproductive outcomes of obese females have not been fully studied. In this study, we aimed to explore the effects and underlying mechanisms of nicotinamide mononucleotide (NMN) on oocyte quality and reproductive performance of obese mice. The obese mouse model was established by feeding high-fat diet which was confirmed by body weight record, fasting blood glucose test and oral glucose tolerance test. The expression of ovary development related genes and inflammation related genes, including Lhx8, Bmp4, Adgre1, Ccl2, TNF-α, Gal-3, Clec10a and IL-10 in ovaries and the expression of Bax and Sod1 in oocytes were detected using quantitative reverse transcription PCR (RT-qPCR). The adipose size of abdominal fat tissue was determined with haematoxylin and eosin (H&E) staining. Immunofluorescence staining was performed to measure the ROS level, spindle/chromosome structure, mitochondrial function, actin dynamics and DNA damage of oocytes. The administration of NMN restored ovarian weight and reduced the adipose size of abdominal fat tissue and ovarian inflammation in high fat diet (HFD) mice. Furthermore, NMN treatment improved the oocytes quality partially by restoring the mitochondrial function and actin dynamics, reducing meiotic defects, DNA damage and ROS level and lipid droplet distribution of oocytes in HFD mice. On the long-term effect, NMN restored offspring body weight of HFD mice. NMN could improve the oocyte quality of HFD-induced obese mice.
Epidermal growth factor receptor (EGFR)-dependent signaling contributes to the pathophysiology of asthma. However, these findings have not been translated into a clinical application. We recently generated ferritin H-chain protein (FTH1)-based nanoparticles with an anti-EGFR single-chain Fv (anti-EGFR scFv) on the surface of FTH1, namely, anti-EGFR scFv-FTH1/FTH1 nanoparticles. In the present study, we found that these nanoparticles could specifically bind to EGFR-expressing cells, leading to downregulation of EGFR and mucin 5AC (MUC5AC) protein expression and growth suppression of House Dust Mite (HDM)-stimulated human bronchial epithelial 16HBE and lipopolysaccharides ()-activated murine macrophage-like RAW264.7 cells. In vivo, intraperitoneal administration of anti-EGFR scFv-FTH1/FTH1 nanoparticles, but not FTH1 nanoparticles, alleviated the major pathological symptoms including airway hyperresponsiveness, airway inflammation, goblet cell hyperplasia, mucus hyperproduction, and increased release of Th2 cytokines in an allergen ovalbumin (OVA)-induced asthma mouse model. Importantly, during the dosing period these nanoparticles were safe for both heathy and asthmatic mice, and more effective in controlling airway inflammation than cetuximab, an EGFR monoclonal antibody. Altogether, our studies provide insights into the control of airway inflammation for treatment of asthma by targeting EGFR. The similar strategy can be used to fabricate scFv-based recombinant protein nanoparticles for other clinical applications.