Association of breast milk-derived arachidonic acid-induced infant gut dysbiosis with the onset of atopic dermatitis.

OBJECTIVE: The specific breast milk-derived metabolites that mediate host-microbiota interactions and contribute to the onset of atopic dermatitis (AD) remain unknown and require further investigation. DESIGN: We enrolled 250 mother-infant pairs and collected 978 longitudinal faecal samples from infants from birth to 6 months of age, along with 243 maternal faecal samples for metagenomics. Concurrently, 239 corresponding breast milk samples were analysed for metabolomics. Animal and cellular experiments were conducted to validate the bioinformatics findings. RESULTS: The clinical findings suggested that a decrease in daily breastfeeding duration was associated with a reduced incidence of AD. This observation inspired us to investigate the effects of breast milk-derived fatty acids. We found that high concentrations of arachidonic acid (AA), but not eicosapentaenoic acid (EPA) or docosahexaenoic acid, induced gut dysbiosis in infants. Further investigation revealed that four specific bacteria degraded mannan into mannose, consequently enhancing the mannan-dependent biosynthesis of O-antigen and lipopolysaccharide. Correlation analysis confirmed that in infants with AD, the abundance of Escherichia coli under high AA concentrations was positively correlated with some microbial pathways (eg, 'GDP-mannose-derived O-antigen and lipopolysaccharide biosynthesis'). These findings are consistent with those of the animal studies. Additionally, AA, but not EPA, disrupted the ratio of CD4/CD8 cells, increased skin lesion area and enhanced the proportion of peripheral Th2 cells. It also promoted IgE secretion and the biosynthesis of prostaglandins and leukotrienes in BALB/c mice fed AA following ovalbumin immunostimulation. Moreover, AA significantly increased IL-4 secretion in HaCaT cells costimulated with TNF-α and INF-γ. CONCLUSIONS: This study demonstrates that AA is intimately linked to the onset of AD via gut dysbiosis.

Influence and mechanism of typical transition metal ions on the denitrification performance of heterotrophic nitrification-aerobic denitrification bacteria.

To investigate the inhibitory effects of various transition metal ions on nitrogen removal and their underlying mechanisms, the single and combined effects of Cu2+ Ni2+ and Zn2+ on Heterotrophic nitrification-aerobic denitrification (HN-AD) bacteria Acinetobacter sp. TAC-1 were studied in a batch experiment system. The results revealed that increasing concentrations of Cu2+ and Ni2+ had a detrimental effect on the removal of ammonium nitrogen (NH4+-N) and total nitrogen (TN). Specifically, Cu2+ concentration of 10 mg/L, the TN degradation rate was 55.09%, compared to 77.60% in the control group. Cu2+ exhibited a pronounced inhibitory effect. In contrast, Zn2+ showed no apparent inhibitory effect on NH4+-N removal and even enhanced TN removal at lower concentrations. However, when the mixed ion concentration of Zn2++Ni2+ exceeded 5 mg/L, the removal rates of NH4+-N and TN were significantly reduced. Moreover, transition metal ions did not significantly impact the removal rates of chemical oxygen demand (COD). The inhibition model fitting results indicated that the inhibition sequence was Cu2+ > Zn2+ > Ni2+. Transcriptome analysis demonstrated that metal ions influence TAC-1 activity by modulating the expression of pivotal genes, including zinc ABC transporter substrate binding protein (znuA), ribosomal protein (rpsM), and chromosome replication initiation protein (dnaA) and DNA replication of TAC-1 under metal ion stress, leading to disruptions in transcription, translation, and cell membrane structure. Finally, a conceptual model was proposed by us to summarize the inhibition mechanism and possible response strategies of TAC-1 bacteria under metal ion stress, and to address the lack of understanding regarding the influence mechanism of TAC-1 on nitrogen removal in wastewater co-polluted by metal and ammonia nitrogen. The results provided practical guidance for the management of transition metal and ammonia nitrogen co-polluted water bodies, as well as the removal of high nitrogen.

Molecular mechanisms of cell death in bronchopulmonary dysplasia.

Bronchopulmonary dysplasia (BPD) in neonates is the most common pulmonary disease that causes neonatal mortality, has complex pathogenesis, and lacks effective treatment. It is associated with chronic obstructive pulmonary disease, pulmonary hypertension, and right ventricular hypertrophy. The occurrence and development of BPD involve various factors, of which premature birth is the most crucial reason for BPD. Under the premise of abnormal lung structure and functional product, newborns are susceptible to damage to oxides, free radicals, hypoxia, infections and so on. The most influential is oxidative stress, which induces cell death in different ways when the oxidative stress balance in the body is disrupted. Increasing evidence has shown that programmed cell death (PCD), including apoptosis, necrosis, autophagy, and ferroptosis, plays a significant role in the molecular and biological mechanisms of BPD and the further development of the disease. Understanding the mode of PCD and its signaling pathways can provide new therapeutic approaches and targets for the clinical treatment of BPD. This review elucidates the mechanism of BPD, focusing on the multiple types of PCD in BPD and their molecular mechanisms, which are mainly based on experimental results obtained in rodents.

Effect mechanism of individual and combined salinity on the nitrogen removal yield of heterotrophic nitrification-aerobic denitrification bacteria.

One of the biggest challenges of applying heterotrophic nitrification-aerobic denitrification (HN-AD) bacteria to treat high salt organic wastewater lies in the inhibitory effect exerted by salinity. To study the inhibition effect and underlying mechanism induced by different ion types and ion composition, the individual and combined effects of NaCl, KCl and Na2SO4 on HN-AD bacteria Acinetobacter sp. TAC-1 were systematically investigated by batch experiments. Results indicated that the ammonia nitrogen removal yield and TAC-1 activity decreased with increased salt concentration. NaCl, KCl and Na2SO4 exerted different degrees of inhibition on TAC-1, with half concentration inhibition constant values of 0.205, 0.238 and 0.110 M, respectively. A synergistic effect on TAC-1 was found with the combinations of NaCl + KCl, NaCl + Na2SO4 and NaCl + KCl + Na2SO4. The whole RNA resequencing suggested that transcripts of denitrification genes (nirB and nasA) were significantly downregulated with increased Na2SO4 concentration. Simultaneously, Na2SO4 stress disrupted cell respiration, DNA replication, transcription, translation, and induced oxidative stress. Finally, we proposed a conceptual model to summarize the inhibition mechanisms and possible response strategies of TAC-1 bacteria under Na2SO4 stress.

A comparative study of microbial community and functions of type 2 diabetes mellitus patients with obesity and healthy people.

The gut microbiota is crucial in the pathogenesis of type 2 diabetes mellitus (T2DM). However, the metabolism of T2DM patients is not well-understood. We aimed to identify the differences on composition and function of gut microbiota between T2DM patients with obesity and healthy people. In this study, 6 T2DM patients with obesity and 6 healthy volunteers were recruited, and metagenomic approach and bioinformatics analysis methods were used to understand the composition of the gut microbiota and the metabolic network. We found a decrease in the abundance of Firmicutes, Oribacterium, and Paenibacillus; this may be attributed to a possible mechanism and biological basis of T2DM; moreover, we identified three critical bacterial taxa, Bacteroides plebeius, Phascolarctobacterium sp. CAG207, and the order Acidaminococcales that can potentially be used for T2DM treatment. We also revealed the composition of the microbiota through functional annotation based on multiple databases and found that carbohydrate metabolism contributed greatly to the pathogenesis of T2DM. This study helps in elucidating the different metabolic roles of microbes in T2DM patients with obesity.

A proof-of-concept study on the effects of low total cfDNA content and solutions to increase the NIPT trisomy 21 detection rate.

BACKGROUND: Non-invasive prenatal testing (NIPT) is routinely used in clinical practice for fetal trisomy screening, but low total cfDNA content and low fetal fraction (LFF) are two factors that affect the detection rate. Samples with low total cfDNA or LFF usually end up with "no-call" results, followed by the blood redraw and re-testing, which is inconvenient for pregnant women and clinicians. METHODS: We created mock trisomy 21 (T21) samples to investigate the effects of low total cfDNA with low LFF and possible solutions to increase their detection rate. RESULTS: Samples with low total cfDNA resulted in the decreased unique reads number and increased duplication rate. Abnormal correlations between library concentration and raw reads number and the coverage fluctuation value, ZsdNorm, were also discovered, suggesting that low total cfDNA could lead to the overestimation of the library concentration. Additionally, a non-reference-based derivative value method (DV method) was evaluated and the data demonstrated that the detection sensitivity of trisomy 21 was increased from 33.33% (6/18) to 94.44% (17/18) in samples with 5% fetal fraction comparing with the z-score approach, whereas for LFF (3.5%) group, the performance was raised from 0% to 35.29% (6/17). CONCLUSION: Low total cfDNA has significant impacts on NIPT performance by altering sequencing quality. The non-reference-based DV method could increase the T21 detection rate in samples with limited cfDNA content and 5% fetal fraction, but it was not as effective for those with LFF.

Associations between Maternal AFP and ß-HCG and Preterm Birth.

OBJECTIVE: Preterm birth (PTB) is a significant public health problem. We aimed to explore whether alpha fetal protein (AFP) or ß-human gonadotropin (ß-HCG) levels during pregnancy were associated with PTB in Chinese population. STUDY DESIGN: The clinical data collected Nanjing Medical University Affiliated Suzhou Hospital and Wuxi Maternity and Child Health Care Hospital between January 2006 and December 2011 were analyzed retrospectively. A total of 64,999 pregnant women were registered. In addition, 13,828 pregnant women were collected serum from the second trimester. The maternal serum AFP and ß-HCG were measured by enzyme immunoassay. RESULTS: In our study, the rate of PTB is 6.23%. With each unit increase of maternal AFP concentration, the adjusted odds of PTB was increased by 69.3% (odds ratio = 1.693, 95% confidence interval: 1.434-1.999, p = 0.00). We set AFP concentrations as high, medium, and low levels. When comparing with low concentration of AFP, high concentration of AFP (≥1.179 M) was positively associated with PTB with adjustment for potential confounders (p < 0.05). Nevertheless, no statistically significant associations were observed between maternal ß-HCG and PTB. CONCLUSION: In this study, maternal AFP concentration was associated with increased risk of PTB.

Vascular endothelial growth factor promotes the activation of hepatic stellate cells in chronic schistosomiasis.

The activation of hepatic stellate cells (HSCs) is a key event in fibrotic pathogenesis. However, the mechanism involving activation of HSCs in chronic schistosomiasis is not entirely clear. Human HSC LX-2 and human umbilical vein endothelial cells (ECs) were cultured with Schistosoma japonicum antigens (SA) in vitro. Fibrosis-associated genes and cell proliferation were analyzed. HSCs were isolated from mice of chronic schistosomiasis with or without praziquantel (PZQ) treatment, followed by the microarray analysis for the liver fibrosis-associated pathways. Although SA inhibited the activation and proliferation of HSCs, it induced the EC proliferation and vascular endothelial growth factor-a (VEGF) production. VEGF significantly increased the proliferation of HSCs and upregulated the expression of collagen and α-smooth muscle actin. For in vivo study, we found that several fibrosis-associated pathways were involved in the HSCs during the reversal of liver fibrosis caused by schistosomiasis, including VEGF, platelet-derived growth factor, tumor necrosis factor and endothelin-1 pathways. The Ingenuity Pathway Analysis showed that VEGF directly regulated several pro-fibrotic and immune cytokine genes in HSCs, including integrin, fibronectin, interferon-γ, interleukin (IL)-6 and IL-10. Our data indicated the critical role of VEGF signaling in HSC activation in chronic schistosomiasis and highlighted several promising genes and pathways in HSCs as potential targets for therapeutic treatment of liver fibrosis.

Activation of the hypothalamic-pituitary-adrenal (HPA) axis contributes to the immunosuppression of mice infected with Angiostrongylus cantonensis.

BACKGROUND: Immunosuppression has been described as a consequence of brain injury and infection by different mechanisms. Angiostrongylus cantonensis can cause injury to the central nervous system and eosinophilic meningitis to human. Both T cell and B cell immunity play an essential role in the resistance of the infection. However, whether brain injury caused by A. cantonensis infection can lead to immunosuppression is not clear. Therefore, the present study sought to observe the alteration of immune responses in mice infected with A. cantonensis. METHODS: Mice were infected with 20 third-stage A. cantonensis larvae. The messenger RNA (mRNA) expression of inflammatory mediators in brain tissues was observed by qRT-PCR. Cell surface markers including CD3, CD4, CD8, CD19, B220, 7-AAD, annexin-V, IgM, AA4.1, and CD23 were evaluated by using flow cytometry. The immune functions of T and B lymphocytes were detected upon stimulation by ConA and antibody responses to a nonself antigen OVA, respectively. Activation of the hypothalamic-pituitary-adrenal axis was evaluated by analyzing the concentration of plasma corticosterone and levels of mRNA for corticotropin-releasing hormone, tyrosine hydroxylase, and c-fos. RESULTS: A. cantonensis infection results in obvious immunosuppression evidenced as progressive spleen and thymus atrophy and significant decrease in the number of lymphocyte subsets including B cells, CD3+ T cells, CD4+ T cells, and CD8+ T cells, as well as reduced T cell proliferation at 21 days post-infection and antibody reaction to exogenous protein after infection. However, the sharp decrease of splenic and thymic cells was not due to cell apoptosis but to B cell genesis cessation and impairing thymocyte development. In addition, helminthicide treatment with albendazole on infected mice at 7 days post-infection could prevent immunosuppressive symptoms. Importantly, infected mice displayed hypothalamic-pituitary-adrenal axis activation, with peak responses occurring at 16 days post-infection, and glucocorticoid receptor antagonist could partially restore the infection-induced cessation of B cell genesis. CONCLUSIONS: Brain injury caused by A. cantonensis infection, like that of brain stroke and trauma, enhanced endogenous corticosteroid activity, resulting in peripheral immunosuppression.

CAPN10 SNP43 G>A gene polymorphism and type 2 diabetes mellitus in the Asian population: a meta-analysis of 9353 participants.

A correlation between the single nucleotide polymorphism (SNP)43 G>A in the calpain-10 (CAPN10) gene (i.e., CAPN10 SNP43) and type 2 diabetes mellitus (T2DM) susceptibility has been suggested, but the evidence for such a relationship remains controversial. To explore the association of the CAPN10 SNP43 with T2DM in Asian populations, a meta-analysis including 9,353 participants from 20 individual studies in Asian populations was conducted. The pooled odds ratios (ORs) and their corresponding 95% confidence intervals (95% CIs) were evaluated by a fixed-effect model or random-effect model. The relationship between CAPN10 SNP43 and T2DM was significant under allelic (OR: 1.18, 95% CI: 1.01-1.38, P = 0.03), recessive (OR: 1.236, 95% CI: 1.038-1.472, P =0.017), heterozygous (OR: 1.261, 95% CI: 1.053-1.512, P = 0.012), and additive (OR: 1.183, 95% CI: 1.014-1.381, P = 0.033) genetic models but not under dominant (OR: 1.12, 95% CI: 0.78-1.62, P = 0.53) or homozygous (OR: 0.937, 95% CI: 0.648-1.355, P = 0.730) genetic models. CAPN10 SNP43 was significantly associated with T2DM susceptibility in Asian populations, especially in Chinese populations. Asians, particularly Chinese people with the SNP43 G allele of the CAPN10 gene may have an increased risk of developing T2DM.

TAP1 I333V gene polymorphism and type 1 diabetes mellitus: a meta-analysis of 2248 cases.

Transporter associated with antigen processing 1 (TAP1) I333V gene polymorphism has been suggested to be associated with type 1 diabetes mellitus (T1DM) susceptibility. However, the results from individual studies are inconsistent. To explore the association of TAP1 I333V gene polymorphisms with T1DM, a meta-analysis involving 2246 cases from 13 individual studies was conducted. The pooled odd ratios (ORs) and their corresponding 95% confidence intervals (95% CIs) were evaluated by a fixed-effect model. A significant relationship was observed between TAP1 I333V gene polymorphism and T1DM in allelic (OR: 1.35, 95% CI: 1.08-1.68, P = 0.007), dominant (OR: 1.462, 95% CI: 1.094-1.955, P = 0.010), homozygous (OR: 1.725, 95% CI: 1.082-2.752, P = 0.022), heterozygous (OR: 1.430, 95% CI: 1.048-1.951, P = 0.024) and additive (OR: 1.348, 95% CI: 1.084-1.676, P = 0.007) genetic models. No significant association between TAP1 I333V gene polymorphism and T1DM was detected in a recessive genetic model (OR: 1.384, 95% CI: 0.743-2.579, P = 0.306) in the entire population, especially among Caucasians. No significant association between them was found in an Asian or African population. TAP1 I333V gene polymorphism was significantly associated with increased T1DM risk. V allele carriers might be predisposed to T1DM susceptibility.

The quantitative and functional changes of NK cells in mice infected with Angiostrongylus cantonensis.

Angiostrongylus cantonensis is a neurotropic parasite which can cause injury to central nervous system and eosinophilic meningitis to human. Natural killer (NK) cells are specialized innate lymphocytes important in early defense against pathogens as in a variety of intracellular bacterial, viral, and protozoan infections. However, the number and function of NK cells in extracellular parasitic infection of A. cantonensis are unclear. In this study, on A. cantonensis infected mice which may mimic the human's infection, we found that the percentage of splenic NK cells and the absolute number of peripheral blood NK cells were decreased at 21-day post infection compared with that of controls. When administrating with albendazole treatment at early stage of the infection, the changes of NK cells could be avoided. Further analysis confirmed that the reduction of NK cells was due to their apoptosis manifested as increased expressions of annexin V and activated caspase-3 after 16-day post infection. Moreover, both activated and inhibitory receptors such as CD16, CD69, NKG2D, and Ly49a on NK cells were down-regulated after 16-day post infection. Interestingly, NK cells isolated from mice of 21-day post infection showed enhanced IFN-γ production when stimulated with IL-12 for 24 h and cytotoxicity to YAC-1 cells, as well as elevated CD107a expression. It is evident that NK cell population and its function were changed in A. cantonensis infected mice, suggesting their involvement in pathogenesis of the infection.

Emerging research themes in maternal hypothyroidism: a bibliometric exploration.

Background: Hypothyroidism, a prevalent endocrine disorder, carries significant implications for maternal and infant health, especially in the context of maternal hypothyroidism. Despite a gradual surge in recent research, achieving a comprehensive understanding of the current state, focal points, and developmental trends in this field remains challenging. Clarifying these aspects and advancing research could notably enhance maternal-infant health outcomes. Therefore, this study employs bibliometric methods to systematically scrutinize maternal hypothyroidism research, serving as a reference for further investigations. Objective: Through bibliometric analysis, this study seeks to unveil key research focus areas, developmental trends, and primary contributors in Maternal Hypothyroidism. The findings offer insights and recommendations to inform future research endeavors in this domain. Methods: Literature metrics analysis was performed on data retrieved and extracted from the Web of Science Core Collection database. The analysis examined the evolution and thematic trends of literature related to Maternal Hypothyroidism. Data were collected on October 28, 2023, and bibliometric analysis was performed using VOSviewer, CiteSpace, and the Bibliometrix software package, considering specific characteristics such as publication year, country/region, institution, authorship, journals, references, and keywords. Results: Retrieved from 1,078 journals, 4,184 articles were authored by 18,037 contributors in 4,580 institutions across 113 countries/regions on six continents. Maternal Hypothyroidism research publications surged from 44 to 310 annually, a 604.54% growth from 1991 to 2022. The USA (940 articles, 45,233 citations), China Medical University (82 articles, 2,176 citations), and Teng, Weiping (52 articles, 1,347 citations) emerged as the most productive country, institution, and author, respectively. "Thyroid" topped with 233 publications, followed by "Journal of Clinical Endocrinology & Metabolism" (202) with the most citations (18,513). "Pregnancy" was the most cited keyword, with recent high-frequency keywords such as "outcome," "gestational diabetes," "iodine intake," "preterm birth," "guideline," and "diagnosis" signaling emerging themes in Maternal Hypothyroidism. Conclusions: This study unveils developmental trends, global collaboration patterns, foundational knowledge, and emerging frontiers in Maternal Hypothyroidism. Over 30 years, research has predominantly focused on aspects like diagnosis, treatment guidelines, thyroid function during pregnancy, and postpartum outcomes, with a central emphasis on the correlation between maternal and fetal health.

Analysis of the evolution of placental oxidative stress research from a bibliometric perspective.

Background: Research on placental oxidative stress is pivotal for comprehending pregnancy-related physiological changes and disease mechanisms. Despite recent advancements, a comprehensive review of current status, hotspots, and trends remains challenging. This bibliometric study systematically analyzes the evolution of placental oxidative stress research, offering a reference for future studies. Objective: To conduct a comprehensive bibliometric analysis of the literature on placental oxidative stress to identify research hotspots, trends, and key contributors, thereby providing guidance for future research. Methods: Relevant data were retrieved from the Web of Science Core Collection database and analyzed using VOSviewer, CiteSpace, and the bibliometrix package. An in-depth analysis of 4,796 publications was conducted, focusing on publication year, country/region, institution, author, journal, references, and keywords. Data collection concluded on 29 April 2024. Results: A total of 4,796 papers were retrieved from 1,173 journals, authored by 18,835 researchers from 4,257 institutions across 103 countries/regions. From 1991 to 2023, annual publications on placental oxidative stress increased from 7 to 359. The United States (1,222 publications, 64,158 citations), the University of Cambridge (125 publications, 13,562 citations), and Graham J. Burton (73 publications, 11,182 citations) were the most productive country, institution, and author, respectively. The journal Placenta had the highest number of publications (329) and citations (17,152), followed by the International Journal of Molecular Sciences (122 publications). The most frequent keywords were "oxidative stress," "expression," "pregnancy," "preeclampsia," and "lipid peroxidation." Emerging high-frequency keywords included "gestational diabetes mellitus," "health," "autophagy," "pathophysiology," "infection," "preterm birth," "stem cell," and "inflammation." Conclusion: Over the past 3 decades, research has concentrated on oxidative stress processes, antioxidant mechanisms, pregnancy-related diseases, and gene expression regulation. Current research frontiers involve exploring pathophysiology and mechanisms, assessing emerging risk factors and environmental impacts, advancing cell biology and stem cell research, and understanding the complex interactions of inflammation and immune regulation. These studies elucidate the mechanisms of placental oxidative stress, offering essential scientific evidence for future intervention strategies, therapeutic approaches, and public health policies.

Quercetin alleviates hyperoxia-induced bronchopulmonary dysplasia by inhibiting ferroptosis through the MAPK/PTGS2 pathway: Insights from network pharmacology, molecular docking, and experimental evaluations.

Quercetin, a bioactive natural compound renowned for its potent anti-inflammatory, antioxidant, and antiviral properties, has exhibited therapeutic potential in various diseases. Given that bronchopulmonary dysplasia (BPD) development is closely linked to inflammation and oxidative stress, and quercetin, a robust antioxidant known to activate NRF2 and influence the ferroptosis pathway, offers promise for a wide range of age groups. Nonetheless, the specific role of quercetin in BPD remains largely unexplored. This study aims to uncover the target role of quercetin in BPD through a combination of network pharmacology, molecular docking, computer analyses, and experimental evaluations.

Efficient modulation of thermal transport in two-dimensional materials for thermal management in device applications.

With the development of chip technology, the density of transistors on integrated circuits is increasing and the size is gradually shrinking to the micro-/nanoscale, with the consequent problem of heat dissipation on chips becoming increasingly serious. For device applications, efficient heat dissipation and thermal management play a key role in ensuring device operation reliability. In this review, we summarize the thermal management applications based on 2D materials from both theoretical and experimental perspectives. The regulation approaches of thermal transport can be divided into two main types: intrinsic structure engineering (acting on the intrinsic structure) and non-structure engineering (applying external fields). On one hand, the thermal transport properties of 2D materials can be modulated by defects and disorders, size effect (including length, width, and the number of layers), heterostructures, structure regulation, doping, alloy, functionalizing, and isotope purity. On the other hand, strain engineering, electric field, and substrate can also modulate thermal transport efficiently without changing the intrinsic structure of the materials. Furthermore, we propose a perspective on the topic of using magnetism and light field to modulate the thermal transport properties of 2D materials. In short, we comprehensively review the existing thermal management modulation applications as well as the latest research progress, and conclude with a discussion and perspective on the applications of 2D materials in thermal management, which will be of great significance to the development of next-generation nanoelectronic devices.

Limosilactobacillus reuteri in immunomodulation: molecular mechanisms and potential applications.

Frequent use of hormones and drugs may be associated with side-effects. Recent studies have shown that probiotics have effects on the prevention and treatment of immune-related diseases. Limosilactobacillus reuteri (L. reuteri) had regulatory effects on intestinal microbiota, host epithelial cells, immune cells, cytokines, antibodies (Ab), toll-like receptors (TLRs), tryptophan (Try) metabolism, antioxidant enzymes, and expression of related genes, and exhibits antibacterial and anti-inflammatory effects, leading to alleviation of disease symptoms. Although the specific composition of the cell-free supernatant (CFS) of L. reuteri has not been clarified, its efficacy in animal models has drawn increased attention to its potential use. This review summarizes the effects of L. reuteri on intestinal flora and immune regulation, and discusses the feasibility of its application in atopic dermatitis (AD), asthma, necrotizing enterocolitis (NEC), systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and multiple sclerosis (MS), and provides insights for the prevention and treatment of immune-related diseases.

Effects of Hydrogen Peroxide-Induced Oxidative Stress on Intestinal Morphology, Redox Status, and Related Molecules in Squabs.

The purpose of this study was to evaluate the potential effect of oxidative stress on the intestine of squabs, and to explore the molecular mechanisms. A total of 360 1-day-old squabs were divided evenly into five different groups (n = 72/group): control, negative control, low, medium, and high dose groups. On the 3rd, 5th, and 7th days, squabs in the control group were not effectively treated and the negative control group were intraperitoneally injected with normal saline, whereas the H2O2 group was injected with H2O2 of 2.0, 2.5, and 3.0 mmol/kg BW respectively. On the 21st day, the serum and duodenum were collected for further analysis. The results indicated that, compared with the control group, H2O2 caused squabs weight loss and intestinal morphology damage, and these effects were enhanced with an increase in dose. Further examination revealed that the contents of oxidative stress markers in both the serum and duodenum of the H2O2 group were significantly enhanced as the dose was increased. In addition, H2O2 exposure also resulted in the lower mRNA expression of Occludin, ZO-1, Beclin1, Atg5, and Caspase-3, but the expression of Claudin2 and Bcl-2 was decreased in comparison to the control group. These findings suggested that duodenal oxidative damage was accompanied by weight loss, changes in intestinal morphology, redox status imbalance, apoptosis as well as autophagy of intestinal cells, with, effects of 3.0 mmol/kg BW of H2O2 being the most severe.

Dietary Dityrosine Induces Oxidative Stress and Mitochondrial-Lipid Imbalance in Mouse Liver via MiR-144-3p-Mediated Downregulation of Nrf2.

SCOPE: Dityrosine (DT) is a protein oxidation marker present in many high-protein foods, such as dairy and meat products. Chronic dietary intake of DT induces oxidative stress damage in the liver and impairs energy metabolism. This study aims to investigate the mechanisms underlying the effects of DT on disrupted hepatic energy metabolism. METHODS AND RESULTS: The study investigates hepatic lipid accumulation, redox status imbalance, mitochondrial dysfunction, and energy metabolism disorders in 4-week-old C57BL/6J mice after 35 days of DT (420 µg kg-1 body weight) treatment. Transcriptome sequencing and quantitative real-time PCR in HepG2 cells show that DT mainly acted via miR-144-3p. miR-144-3p targets immune responsive gene 1 (IRG1) and decreases the fumaric acid level in the tricarboxylic acid (TCA) cycle, thereby decreasing nuclear factor erythroid 2-related factor 2 (Nrf2) expression and antioxidant activity. CONCLUSION: Administration of lycopene, a strong antioxidant, alleviates DT-induced damage in mice, confirming the involvement of the Nrf2 pathway in DT-induced abnormal hepatic lipid metabolism and energy homeostasis.

Lactobacillus for the treatment and prevention of atopic dermatitis: Clinical and experimental evidence.

Atopic dermatitis (AD) is a chronic inflammatory skin disease, accompanied by itching and swelling. The main pathological mechanism of AD is related to the imbalance between Type 2 helper cells (Th2 cells) and Type 1 helper cells (Th1 cells). Currently, no safe and effective means to treat and prevent AD are available; moreover, some treatments have side effects. Probiotics, such as some strains of Lactobacillus, can address these concerns via various pathways: i) facilitating high patient compliance; ii) regulating Th1/Th2 balance, increasing IL-10 secretion, and reducing inflammatory cytokines; iii) accelerating the maturation of the immune system, maintaining intestinal homeostasis, and improving gut microbiota; and iv) improving the symptoms of AD. This review describes the treatment and prevention of AD using 13 species of Lactobacillus. AD is commonly observed in children. Therefore, the review includes a higher proportion of studies on AD in children and fewer in adolescents and adults. However, there are also some strains that do not improve the symptoms of AD and even worsen allergies in children. In addition, a subset of the genus Lactobacillus that can prevent and relieve AD has been identified in vitro. Therefore, future studies should include more in vivo studies and randomized controlled clinical trials. Given the advantages and disadvantages mentioned above, further research in this area is urgently required.