Impaired Immune Function Research Articles

Recent Progress of the Membrane Palmitoylated Protein (MPP)

Mycoplasma pneumoniae (MP) is a common pathogen that causes acquired pneumonia. MPP is a relatively common respiratory disease, which can be spread through droplets and direct contact in crowded environments. Smokers, infants and people with low immunity are high-risk groups, and the incidence of MPP is increasing year by year under the influence of environmental factors and impaired immune function. Understanding its pathogenesis and identifying predictive biomarkers, while assisting blood or imaging tests, is one of the hot spots of clinicians' attention. At the same time, comprehensive measures should be adopted for the treatment of MPP, because although the disease is often considered to be a self-limiting disease, with the in-depth study of the disease, it is found that drug-resistant mycoplasma pneumoniae strains are gradually increasing, the incidence of severe or refractory mycoplasma pneumoniae pneumonia is also increasing, and the difficulty of clinical treatment is also increasing. This text will talk about the history of MMP and the common symptoms and signs associated with the infection, including cough, fever, sore throat, fatigue, and other respiratory symptoms. Also, it covers the diagnostic methods used to identify MMP. Finally,this paper discuss the efficacy of different treatment options, including antibiotics commonly used to treat MMP, covering the safety of these treatments, including any potential side effects or contraindications. Additionally, it explores the potential resistance of MMP to different antibiotics and how this resistance might affect treatment outcomes.

The impact of COVID-19 on accelerating of immunosenescence and brain aging

The COVID-19 pandemic, caused by the novel coronavirus SARS-CoV-2, has profoundly impacted global health, affecting not only the immediate morbidity and mortality rates but also long-term health outcomes across various populations. Although the acute effects of COVID-19 on the respiratory system have initially been the primary focus, it is increasingly evident that the virus can have significant impacts on multiple physiological systems, including the nervous and immune systems. The pandemic has highlighted the complex interplay between viral infection, immune aging, and brain health, that can potentially accelerate neuroimmune aging and contribute to the persistence of long COVID conditions. By inducing chronic inflammation, immunosenescence, and neuroinflammation, COVID-19 may exacerbate the processes of neuroimmune aging, leading to increased risks of cognitive decline, neurodegenerative diseases, and impaired immune function. Key factors include chronic immune dysregulation, oxidative stress, neuroinflammation, and the disruption of cellular processes. These overlapping mechanisms between aging and COVID-19 illustrate how the virus can induce and accelerate aging-related processes, leading to an increased risk of neurodegenerative diseases and other age-related conditions. This mini-review examines key features and possible mechanisms of COVID-19-induced neuroimmune aging that may contribute to the persistence and severity of long COVID. Understanding these interactions is crucial for developing effective interventions. Anti-inflammatory therapies, neuroprotective agents, immunomodulatory treatments, and lifestyle interventions all hold potential for mitigating the long-term effects of the virus. By addressing these challenges, we can improve health outcomes and quality of life for millions affected by the pandemic.

The anti-inflammatory cytokine interferon-gamma as a potential therapeutic target of Alzheimer’s disease: a retrospective observational study

The age-related neurodegenerative disease Alzheimer’s disease is characterized by progressive cognitive decline and neurodegeneration and is often accompanied by inflammation within the central nervous system. This study investigated the role of interferon-gamma, an anti-inflammatory cytokine, in Alzheimer’s disease pathogenesis. Our findings highlight three critical insights: first, there was a significant reduction in interferon-gamma expression at the early stages of Alzheimer’s disease, suggesting an initial impairment in immune function. Second, we identified a novel correlation between the expression levels of interferon-gamma and its receptors, which may indicate a mechanism through which interferon-gamma signaling is altered in Alzheimer’s disease. Third, we observed an increase in entropy and determinant values for interferon-gamma and its receptors, suggesting that systemic dysregulation likely contributes to disease progression. Our study underscores the pivotal role of interferon-gamma in Alzheimer’s disease and highlights its potential as a therapeutic target.

The Immunosuppressive Functions of Eosinophils Are Compromised in Patients With Allergic Rhinitis, Particularly Concerning Rab27a Expression.

Eosinophils have been acknowledged to be involved in the induction of numerous inflammatory disorders. There is still a lack of knowledge about whether eosinophils play a role in immune regulation. The aim of this study is to uncover the immune regulatory functions of eosinophils. Blood samples were collected from patients with allergic rhinitis (AR) and healthy control subjects. Peripheral blood mononuclear cells (PBMCs) were isolated from blood samples. Eosinophils were purified from PBMCs using flow cytometry cell sorting and analyzed using immunological approaches. The results showed that eosinophils from healthy subjects had immune regulatory functions on T cell proliferation and cytokine release. Impairment of eosinophil immune regulatory functions was found in AR patients, which was associated with AR responses. Elevated Rab27a expression in eosinophils was associated with their impaired immune regulatory functions and the increased AR responses. Rab27a controlled the release of mediators from eosinophils. Low concentrations of Eosinophil mediators could trigger immune regulatory responses, while high concentrations could trigger inflammatory responses. Regulating Rab27a restored the immune regulatory functions of eosinophils of AR patients. Eosinophils have immune regulatory functions, which are controlled by the expression of Rab27a. Regulation of Rab27a can improve the immune regulatory functions of eosinophils. The data suggest that inhibition of Rab27a can be a drug candidate for the treatment of eosinophil-related disorders.

Impaired hemostatic and immune functions of platelets after acute thrombocytopenia.

Platelets are pivotal in maintaining vascular integrity, hemostasis, and immune modulation, with newly generated, immature platelets being the most responsive in fulfilling these tasks. Therefore, the immature platelet fraction provides insights into thrombopoiesis dynamics and clinical prognostication. However, it is currently unclear how immature platelet functions change in settings of acute thrombocytopenia. We aimed to investigate the functional consequences of acute thrombocytopenia on newly generated immature platelets in various mouse models and human subjects. To examine platelet functionality after acute thrombocytopenia, we depleted either megakaryocytes using a platelet factor 4-specific inducible diphtheria toxin receptor transgenic mouse model or platelets via antibody-mediated depletion in mice, and collected blood from acute myeloid leukemia (AML) patients before and after consolidation or induction chemotherapy. Chemotherapy treatment was further repeated in an animal model. We assessed surface receptor expression of activation markers (CD62P, active GPIIb/IIIa, CD40L, CD63, CD107a) and toll-like receptors (TLR2, TLR4, TLR9) on immature and mature platelets following activation. Additionally, we investigated procoagulant platelet formation and platelet-leukocyte interactions in mouse models and patients with AML. In murine models, acute thrombocytopenia led to impaired hemostatic function and altered surface receptor expression in newly generated immature platelets. Similarly, AML patients during regeneration post chemotherapy exhibited reduced platelet activation and procoagulant function, alongside altered receptor expression and diminished platelet-leukocyte interactions. After acute thrombocytopenia platelet-mediated hemostasis and immune modulation by newly generated platelets are impaired, underscoring the clinical relevance of understanding platelet function alterations in (post)thrombocytopenic conditions for therapeutic optimization.

Zearalenone delays tissue regeneration by dysregulating neutrophil balance in zebrafish (Danio rerio) larvae.

Zearalenone (ZEA), a common mycotoxin, poses significant environmental and health risks. While its toxicological effects are well-studied, its impact on regeneration remains unclear. This study explored ZEA's effects on zebrafish (Danio rerio) larvae, focusing on developmental toxicity, immunotoxicity, and tissue regeneration. Embryos were exposed to 0, 0.5, 1, and 1.5μM ZEA from 6 to 72 h post-fertilization (hpf). Although hatching and survival rates remained unaffected, malformations, including body axis bending and pericardial edema, increased dose-dependently, with 4.44% abnormalities observed at 1.5μM (p=0.01). Heart rates also declined significantly at 1.5μM (75.40 vs. 72.53 beats/30s, p=0.0054). Immunotoxicity was assessed using Tg(mpx: eGFP) zebrafish to monitor neutrophil responses post-injury. ZEA exposure led to increased neutrophil counts (229.87 vs. 330.80, p<0.0001) and chemotaxis (21.15% vs. 34.57%, p<0.0001). RNA sequencing of 0 and 1.5μM groups revealed disrupted redox balance and oxygen transport, with down-regulation of hbae1, hbbe2, and hbae3 and up-regulation of hif1a, indicating hypoxia involvement. Elevated reactive oxygen species (ROS), reduced antioxidant enzyme activity, and increased apoptosis were also observed. Tail fin regeneration assays showed delayed regeneration at 1 and 1.5μM ZEA, linked to impaired immune function and oxidative stress. These findings highlight ZEA's adverse effects on developmental and regenerative processes, underscoring its environmental and health implications and the need for further research.

Are HFPO-TA and HFPO-DA safe substitutes for PFOA? A comprehensive toxicity study using zebrafish (Danio rerio) embryos and adults

Due to the multiple biotoxicity caused by perfluorooctanoic acid (PFOA), the application and production of PFOA is regulated globally. PFOA substitutes including hexafluoropropylene oxide trimer acid (HFPO-TA) and hexafluoropropylene oxide dimer acid (HFPO-DA) have been applied to industrial processes and subsequently detected in surface and groundwater, yet there is a lack of comprehensive assessment of their toxicity to aquatic organisms. Therefore, under the same time and same experimental conditions, the toxic effects and differences of PFOA, HFPO-TA, and HFPO-DA on zebrafish adults and embryos were assessed from oxidative damage, apoptosis, immune function impairment, and protein interactions. The HFPO-TA and HFPO-DA caused more severe oxidative damage than PFOA. While PFOA only disrupted immune function in adults, HFPO-TA and HFPO-DA affected immune homeostasis in both adults and embryos. Integrated biomarker response results showed that superoxide dismutase (SOD) activity and reactive oxygen species content could be used as early warning indicators of toxicity in adults and embryos, respectively. Molecular docking simulations identified HFPO-TA as having the lowest binding energy with SOD proteins, thereby exerting the greatest effect on SOD activity. Compared to PFOA, HFPO-TA and HFPO-DA exhibited a greater toxicological response and, therefore, may not be suitable substitutes for PFOA.

The impact of surgical time of day and surgical site infection.

Disruption to the circadian clock has impacts on health and wellbeing, including impaired immune function and wound healing. It is plausible that the timing of surgical procedures could impact the body's response to trauma and susceptibility to infections. Using the Health Quality & Safety Commission data on surgical site infections (SSI) we sought to investigate any possible time of day effects on the incidents of recorded infections. All recorded data from June 2017 to July 2021 were extracted for cardiac and orthopaedic operations in New Zealand. The incidence of SSI was calculated for each 4-hour bin of time across the day. There was a total of 87,034 cases in the analysis, of which 1,327 (1.5%) had an infection. Univariately, there was a significant time of day effect, with operations after 8 pm being 3.91 times more likely to have an infection (p<0.001), and operations between 4 pm and 8 pm being 0.71 times more likely (p=0.03) to have an infection compared to operations conducted between 12 pm and 4 pm. However, when age, acuity and American Society of Anesthesiologists score were included in the model, there were no differences in the rate of infection by time of day. This preliminary work suggests that surgical time of day does not significantly impact incidence of surgical infection when other variables are controlled for. However, this work has not considered other factors that may also be important. We plan to link the SSI data with the National Minimum Dataset to investigate these other factors and conduct a more comprehensive analysis.

Cannabidiol, a Strategy in Aging to Improve Redox State and Immunity in Male Rats.

Aging is characterized by oxidative stress and immune function impairment, and is associated with increased morbidity. Cannabidiol (CBD) has anti-oxidant properties, but its role in aging has been scarcely studied. This work aims to test the effect of CBD on the redox state and immunity during aging in rats. In this study, 15-month-old male Long Evans rats received 10 mg/kg b.w/day of CBD in their diet for 10 weeks and were compared with same-age control and 2-month-old rats serving as a young control group, both following a standard diet. After treatment, they were sacrificed, and the spleen, thymus, and total blood cells were collected. Redox parameters such as glutathione reductase and peroxidase activities, reduced (GSH) and oxidized (GSSG) glutathione concentration, GSSG/GSH ratio, and lipid peroxidation were evaluated. Moreover, immune functions (chemotaxis, natural killer activity, and lymphoproliferation) were analyzed in the spleen. Results show that the 15-month-old control rats exhibited increased oxidative stress and immunosenescence compared to the 2-month-old rats. However, the CBD-treated animals showed higher anti-oxidant defenses, lower oxidants in the spleen, thymus, and blood cells, and better immunity in the spleen than the corresponding age-matched controls. Therefore, CBD administration neutralizes oxidative stress and improves immunity, suggesting it is a strategy for achieving healthy aging.

Risk factors for surgical site infection after general surgery in HIV-infected patients: a retrospective study

BackgroundAs the number of HIV-infected patients increased, the number of patients requiring general surgery has subsequently increased. However, impairment of immune function due to HIV infection increases the risk of postoperative surgical-site infection and significant harm to patient health. This study aimed to examine the risk factors for surgical-site infection after general surgery.MethodsThe patients’ data were from Zunyi fourth hospital medical information system. Machine learning based Boruta algorithm were used for variable screening. Univariable and multivariable logistic regression and restricted cubic spline analysis were performed to examine the relationship between significant variables and surgical-site infection.ResultsA total of 125 general surgery postoperative HIV-infected patients participated in the study. Surgical-site pathogen culture identified Escherichia coli, Klebsiella pneumoniae, and mixed bacteria as the three most common pathogens causing Surgical-site infection. Univariable and multivariable logistic regression analysis to adjust for risk factors identified type III surgical incision (OR = 9.92, 95% CI = 1.28–76.75) and elevated preoperative white blood cell (WBC) count (OR = 1.30, 95% CI = 1.12–1.51) as independent risk factors for postoperative surgical-site infection, whereas CD4 + T lymphocyte count greater than 400 cells/µL was identified as a protective factor (OR = 0.23, 95% CI = 0.09–0.60) while. The restricted cubic spline analysis results directly reflected the dose-response relationship between continuous variables and postoperative surgical-site infection.ConclusionsType III incision and an elevated WBC count pose a higher risk of postoperative surgical-site infection. A CD4 + T lymphocyte counts greater than 400 cells/µL provided a protective effect of lower risk of surgical site infection. Preoperative serum neutrophil percentage, albumin level, red blood cell count, and serum urea level within a specific range were beneficial in reducing the risk of incisional infections. Our research provides a theoretical basis for clinical practice.

Ocean acidification aggravates the toxicity of deltamethrin in Haliotis discus hannai: Insights from immune response, histopathology and physiological responses

Ocean acidification (OA) and other environmental factors can collectively affect marine organisms. Deltamethrin (DM), a type II pyrethroid insecticide, has been widely detected in coastal and estuarine areas, while little attention has been given to the combined effects of DM and OA. In this study, Haliotis discus hannai was exposed to three pH levels (8.1, 7.7 and 7.4) and three DM nominal concentrations (0 μg/L, 0.6 μg/L and 6 μg/L) for 14 and 28 days. The results indicated that experimental acidification and/or DM exposure led to impaired immune function and pathological damage. Additionally, acidified conditions and DM exposure induced oxidative stress, and gills are more sensitive than digestive glands. With increasing pCO2 and DM nominal concentrations, superoxide dismutase (SOD) activity decreased, whereas catalase (CAT) and glutathione S-transferase (GST) activities increased in the gills. Moreover, the expression levels of Toll-like receptor (TLR) pathway-related genes were upregulated after exposure. Integrated biomarker response (IBR) analysis proved that acidified conditions and/or DM detrimentally affected the overall fitness of H. discus hannai, and co-exposure to experimental acidification and DM was the most stressful condition. This study emphasizes the necessity of incorporating OA in future pollutant environmental assessments to better elucidate the risks of environmental disturbance.

"No Medication Means No HIV Diagnosis": A Qualitative Study Based on Dual-System Theory on HIV Antiretroviral Therapy Initiation Decision-Making.

At least 30% of newly diagnosed people living with HIV (PLHIV) have delayed antiretroviral therapy (ART) initiation globally, resulting in irreversible impaired immune function and increased risk of HIV transmission. This study aimed to explore the decision-making process of ART initiation in China. A phenomenological research design was used and semi-structured, in-depth interviews based on dual-system theory were conducted. Participants were selected using purposive sampling between December 11, 2021 and June 25, 2022. Interpretative phenomenological analysis (IPA) was performed utilizing the software NVivo 12. A total of 34 PLHIV were interviewed. The heuristic system and the analytic system were involved in the complex decision-making process for ART initiation. Acceptability, negative emotion, and stigma were all parts of the heuristic system. The analytic system included the perception of ART benefits, positive support, and misconception. Two systems interacted with each other in the decision-making of ART initiation. PLHIV's initiation decision was determined by the components of the dominant system. This theory-driven qualitative study provided valuable insights on the decision-making process of ART initiation among newly diagnosed PLHIV.

Autoimmune and Neoplastic Outcomes After the mRNA Vaccination: The Role of T Regulatory Cell Responses

A plethora of autoimmune disease incidences occured after COVID-19 mRNA injections were rolled out. Aggressive cancer cases have occurred in the bodies of recipients at sites where the mRNA was injected and at distant metastatic sites. The mRNA vaccines cause thymic involution (shrinking) and dysregulation of the T regulatory (Treg) and T effector (Teff) homeostatic cell balance. Activated immune cells deliver spike protein to the thymic epithelial cells, damaging them. The Treg/Teff balance may determine the fate of autoimmunity and/or cancer and is different for patients with cancer versus those without any cancerous tissues. Repeated mRNA injections lead to empirical evidence of impaired immune functions (elevated IgG4, PD-L1), associated with increased autoimmunity and cancer risks, and decreased resistance to infections. In the with-cancer recipients, the mRNA vaccine may be associated with either autoimmunity or further progression of the cancer(s) depending on the immunotherapy treatment the patient receives. When an antigen stimulates the immune system, specific T regulatory (Treg) and T effector (Teff) subpopulations develop from naïve T cells. An imbalance between Treg and Teff cells can lead to either cancer or autoimmunity. Treg cells are beneficial in that they protect from autoimmunity. However, they suppress the immune response to tumors. In this review, we analyze Treg responses after SARS-CoV-2 mRNA vaccination and find distinct pathological responses under differing conditions. Injection with modified mRNA can lead to a delayed but highly active immune response, resulting in overactivation of the inflammasome. The mRNA “vaccine” induces a very strong IgG antibody response, while suppressing CD8+ T cell activation. Exosomes distribute the recombinant, synthetic spike protein and the mRNA encoding it throughout the organism. In cancer patients, disease progression depends on the starting point of the cancer patient at the time of injection and the type of cancer treatment underway. Migration of circulating dendritic cells and Treg cells back to the thymus, while they are carrying spike protein, damages the medullary thymic epithelial cells and accelerates thymic involution, a direct cause of inflammaging and immunosenescence. In summary, the Treg responses to mRNA injections and subsequent mRNA-encoded SARS-CoV-2 spike protein expression may disrupt immune capacities resulting in accelerated development of autoimmune disease and cancer. The processes discussed here are consistent with both epidemiological findings and case reports.

Inborn Errors of Immunity in Pediatric Intensive Care: Prevalence, Characteristics, and Prognosis.

Inborn errors of immunity (IEI) are a heterogeneous group of genetic diseases characterized by impaired immune system function. This prospective study aimed to determine the frequency, characteristics, and clinical course of IEI patients admitted to the pediatric intensive care unit (PICU) and identify mortality-related factors. Using a comprehensive immunological evaluation protocol, we screened 753 PICU admissions for potential IEIs during three years. Patients with pre-existing IEI diagnoses, chronic diseases, ongoing chronic medication regimens, other known comorbidities, trauma cases, post-surgical cases, and poisonings were excluded. Thirty-three patients were newly diagnosed with IEIs during or as a result of their PICU stay, representing an incidence of 4.39%. The most common disorders were immunodeficiencies with immune dysregulation (48.5%), followed by combined immunodeficiencies (24.2%). Severe viral infections (61%) and life-threatening infections (51.7%) were the most frequent warning signs. Only 31% of patients exhibited at least two Jeffrey Modell Foundation warning signs. The mortality rate was 58%, highlighting the need for early diagnosis and treatment. Newborn screening and family segregation studies are crucial to improving outcomes for IEI patients in intensive care settings.

Dysregulation of epigenetic modifications in inborn errors of immunity.

Inborn errors of immunity (IEIs) are a group of typically monogenic disorders characterized by dysfunction in the immune system. Individuals with these disorders experience increased susceptibility to infections, autoimmunity and malignancies due to abnormal immune responses. Epigenetic modifications, including DNA methylation, histone modifications and chromatin remodeling, have been well explored in the regulation of immune cell development and effector function. Aberrant epigenetic modifications can disrupt gene expression profiles crucial for immune responses, resulting in impaired immune cell differentiation and function. Dysregulation of these processes caused by mutations in genes involving in epigenetic modifications has been associated with various IEIs. In this review article, we focus on IEIs that are caused by mutations in 13 genes involved in the regulation of DNA methylation, histone modification and chromatin remodeling.

Mitigating sTNF/TNFR1 activation on VGluT2 + spinal cord interneurons improves immune function after mid-thoracic spinal cord injury

Spinal cord injury (SCI) is a devastating condition with 250,000 to 500,000 new cases globally each year. Respiratory infections, e.g., pneumonia and influenza are the leading cause of death after SCI. Unfortunately, there is a poor understanding of how altered neuro-immune communication impacts an individual’s outcome to infection. In humans and rodents, SCI leads to maladaptive changes in the spinal-sympathetic reflex (SSR) circuit which is crucial to sympathetic function. The cause of the impaired immune function may be related to harmful neuroinflammation which is detrimental to homeostatic neuronal function, aberrant plasticity, and hyperexcitable circuits. Soluble tumor necrosis factor (sTNF) is a pro-inflammatory cytokine that is elevated in the CNS after SCI and remains elevated for several months after injury. By pharmacologically attenuating sTNF in the CNS after SCI we were able to demonstrate improved immune function. Furthermore, when we investigated the specific cellular population which may be involved in altered neuro-immune communication we reported that excessive TNFR1 activity on excitatory INs promotes immune dysfunction. Furthermore, this observation is NF-kβ dependent in VGluT2 + INs. Our data is the first report of a target within the CNS, TNFR1, that contributes to SCI-induced immune dysfunction after T9-SCI and is a potential avenue for future therapeutics.

Association between red blood cells transfusion and 28-day mortality rate in septic patients with concomitant chronic kidney disease

Patients with chronic kidney disease (CKD) often have impaired immune function, making them more prone to infections that can lead to sepsis. The coexistence of these conditions can result in decreased hemoglobin levels and is associated with a higher mortality rate. To investigate whether the transfusion of red blood cells (RBCs) improves the prognosis of septic patients with concomitant CKD and to explore the indications for red blood cell transfusion. This retrospective cohort study utilizes data from the MIMIC-IV (v2.0) database. The study enrolled 6,604 patients with sepsis and concomitant CKD admitted to the Intensive Care Unit (ICU). Propensity score matching (PSM) was applied to adjust for confounding factors. Multivariate Cox regression analysis revealed an association between RBC transfusion and a decreased risk of 28-day mortality (HR: 0.61, 95% CI: 0.54–0.70, P < 0.001). Following a meticulous 1:1 propensity score matching analysis between the two cohorts, the matched population revealed a notable decrease in 28-day mortality within the RBC transfusion group (HR: 0.60, 95% CI: 0.51–0.71; P < 0.001). Additionally, we observed that a SOFA score ≥ 5, a Base Excess (BE) value < 3, and an estimated Glomerular Filtration Rate (eGFR) < 30 may be considered when evaluating the potential need for RBC transfusion. This study demonstrated an association between RBC transfusion and decreased 28-day mortality in patients with sepsis accompanied by CKD. The patient’s BE value, SOFA score, and eGFR are crucial factors influencing the treatment outcome and should be considered when deciding on RBC transfusion.

The Immune Regulatory Functions in B Cells Are Restored by CpG to Reduce Experimental Food Allergy.

Dysfunctional immune regulation contributes to the pathogenesis of food allergy (FA). The mechanism behind regulatory B-cell dysfunction is unclear. CpG has immune regulatory functions. The purpose of this study is to use CpG to recover the immune suppressive functions of B cells in mice with FA. An FA mouse model was created using ovalbumin as the specific antigen. Flow cytometry was used to isolate B cells from the intestinal tissues. The immune regulatory functions of B cells were assessed using immunological approaches. The results showed that the FA response was linked to low IL-10 levels in gut lavage fluids of FA mice. FA mouse intestinal B cells produced lower amounts of IL-10 as compared with B cells isolated from naïve control mice. Impaired immune suppressive functions were observed in B cells isolated from the FA mouse intestine. The inducibility of the Il10 expression in naïve B cells of the intestine of FA mice was defective. The induction of Il10 expression in FA B cells could be restored by CpG through regulating the methylation status of the Cmip promoter. CpG promoted the therapeutic efficacy of allergen specific immunotherapy by restoring the induction of IL-10+ B cells in the intestine. The expression of Il10 in B cells of the FA mouse intestine was impaired. Administration of CpG could restore the expression of Il10 in B cells in the intestine and promote immunotherapy for FA.

Reproduction results in parallel changes of oxidative stress and immunocompetence in a wild long-living mammal-edible dormouse Glis glis.

Oxidative stress (OS) and impaired immune function (IF) have been proposed as key physiological costs of reproduction. The relationship between OS and IF remains unresolved, particularly in long-living iteroparous species. We studied physiological markers of maintenance (OS, IF markers) in lactating, post-lactating and non-lactating females of edible dormice-a long-living rodent. We predicted the OS balance and IF to be compromised by lactation, especially in older females expected to face stronger trade-offs between life functions. We found that the age predictor (body size) correlated negatively with white blood cell level (WBC), positively with neutrophils to lymphocytes ratio and had no effect on OS markers. Oxidative damage markers (reactive oxygen metabolites (ROMs); but not antioxidant capacity) and body size-adjusted WBC were the lowest in lactating, higher in post-lactating and the highest in non-lactating females. Body size/age did not affect this correlation suggesting a similar age-independent allocation strategy during reproduction in this species. The path analysis testing the causal relationship between ROMs and WBC revealed that IF is more likely to affect OS than vice versa. Our study indicates the trade-off between crucial life functions during reproduction and suggests that immunosuppression reduces the risk of OS; therefore, mitigating oxidative costs of reproduction.

Antioxidant Vitamin B Group Supplementation Induces Immune Function, Glycemic Control, and Reduces Infection Risk in Type 2 Diabetes Mellitus: A Randomized Controlled Trial

Background: Diabetes mellitus is associated with impaired immune function and increased susceptibility to infections, with oxidative stress and inflammation playing significant roles in disease progression. Micronutrient deficiencies, particularly in antioxidants, are common among diabetic patients and may exacerbate these complications. This study aimed to evaluate the impact of antioxidant vitamin supplementation on oxidative stress, inflammation, and infection frequency in diabetic patients. Methods: This randomized, placebo-controlled study enrolled diabetic patients from multiple centers and assigned them to either a supplementation group receiving specific doses of vitamins (including vitamins C, E, and B complex) or a placebo group. Baseline data included demographic, clinical, and biochemical characteristics. Plasma antioxidant levels, inflammatory markers, and infection frequencies were assessed at baseline, three months, and twelve months for long-term effects. Statistical analyses compared group differences over time and assessed the association between supplementation and clinical outcomes. Results: At three months, patients in the supplementation group showed significant increases in plasma antioxidant levels and reductions in inflammatory markers compared to the placebo group (p &lt; 0.05). Frequencies of infections over the initial three-month period were lower in the treatment group (15%) compared to the placebo (25%) (p &lt; 0.05). Over the twelve-month follow-up, infection rates continued to be lower in the treatment group (20% vs. 30%), indicating a sustained effect of supplementation on infection risk in diabetic patients. Conclusion: Antioxidant vitamin supplementation in diabetic patients significantly improved plasma antioxidant levels, reduced inflammatory markers, and was associated with a lower incidence of infections over both short and long-term follow-ups.