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Featured Application: This work provides a detailed exploration of pollen–food allergy syndrome (PFAS), offering practical insights for clinicians managing patients with this condition. By addressing the diagnostic challenges and discussing emerging therapeutic approaches, including allergen immunotherapy and biologics, the findings have potential applications in improving diagnostic accuracy and optimizing personalized treatment strategies. The work could also guide future research on innovative management techniques and promote awareness among healthcare providers dealing with allergic diseases. Pollen–food allergy syndrome (PFAS), also known as oral allergy syndrome, is a common condition affecting individuals sensitized to pollens such as birch, ragweed, and grass. This syndrome arises from immunological cross-reactivity between pollen allergens and structurally similar proteins found in various fruits, vegetables, and nuts. Although typically presenting with mild oral and pharyngeal symptoms, PFAS can occasionally result in severe allergic reactions, underscoring its clinical significance. This review explores the pathophysiology of PFAS, highlighting the molecular mechanisms underlying cross-reactivity and examining the main protein families involved, including those contributing to variations in symptom severity. Current diagnostic approaches, including skin prick testing, specific immunoglobulin E measurements, and component-resolved diagnostics, are discussed. Emerging diagnostic tools and biomarkers with potential to enhance accuracy are also examined. Therapeutic strategies for PFAS primarily focus on symptom management and avoidance of trigger foods. However, novel approaches such as allergen immunotherapy and biologics targeting key immune pathways are gaining traction as potential interventions for more severe or refractory cases. By addressing the diagnostic and therapeutic challenges of PFAS, this paper aims to provide clinicians and researchers with a comprehensive understanding of this condition, fostering improved patient care and the development of innovative treatment strategies. [ABSTRACT FROM AUTHOR]

Background: A growing body of evidence links a high-fructose diet (HFrD) to metabolic disturbances, including inflammation, dyslipidemia, insulin resistance and also endothelial dysfunction, yet its role in allergic asthma remains underexplored. Considering that obesity and hypercholesterolemia exacerbate asthma by promoting systemic inflammation, investigating interventions with dual metabolic and anti-inflammatory effects is essential. This study aimed to evaluate the potential modulatory effects of rosuvastatin in ameliorating the effects of HFrD-induced metabolic and vascular dysfunction in the context of allergic asthma. Methods: Forty-eight Sprague-Dawley rats were assigned to eight groups, receiving either a standard or HFrD for 12 weeks. Allergic asthma was induced using an ovalbumin sensitization and challenge protocol, while controls were administered saline. Selected groups were treated with rosuvastatin throughout the entire duration of the experiment. Body weight, abdominal circumference and serum biomarkers were assessed at baseline, 6 and 12 weeks. Endothelial function was assessed by evaluating vascular reactivity in an isolated organ bath. Additionally, histopathological analyses of aortic and pulmonary tissues were conducted to investigate inflammatory responses and morphological changes. Results: Rats on HFrDs exhibited significant increases in body weight, abdominal circumference, lipid profiles and blood glucose, which were further aggravated by allergic asthma. Rosuvastatin treatment notably reduced lipid levels, C-reactive protein and immunoglobulin E, while also enhancing vascular reactivity and attenuating aortic and bronchial wall thickening. Conclusions: Our findings suggest that rosuvastatin may serve as an effective therapeutic agent for addressing vascular and inflammatory complications associated with a high fructose intake and allergic asthma. [ABSTRACT FROM AUTHOR]

Recurrent pregnancy loss (RPL) is a complex early pregnancy complication affecting 1–2% of couples and is often linked to immune dysfunction. Aberrations in T and B cell subpopulations, as well as natural killer (NK) cell activity, are particularly influential, with studies showing that abnormal NK cell activation and imbalances in T and B cell subtypes contribute to immune-mediated miscarriage risk. Successful pregnancy requires a tightly regulated balance between pro-inflammatory and anti-inflammatory immune responses. In the early stages, inflammation supports processes such as trophoblast invasion and spiral artery remodeling, but this must be tempered to prevent immune rejection of the fetus. In this review, we explore the underlying immune mechanisms of RPL, focusing on how dysregulated T, B, and NK cell function disrupts maternal tolerance. Specifically, we discuss the essential role of uterine NK cells in the early stages of vascular remodeling in the decidua and regulate the depth of invasion by extravillous trophoblasts. Furthermore, we focus on the delicate Treg dynamics that enable the maintenance of optimal immune homeostasis, where the balance, and not only the quantity of Tregs, is crucial for fostering maternal–fetal tolerance. Other T cell subpopulations, such as Th1, Th2, and Th17 cells, also contribute to immune imbalance, with Th1 and Th17 cells promoting inflammation and potentially harming fetal tolerance, while Th2 cells support immune tolerance. Finally, we show how changes in B cell subpopulations and their functions have been associated with adverse pregnancy outcomes. We further discuss current therapeutic strategies aimed at correcting these immune imbalances, including intravenous immunoglobulin (IVIg), glucocorticoids, and TNF-α inhibitors, examining their efficacy, challenges, and potential side effects. By highlighting both the therapeutic benefits and limitations of these interventions, we aim to offer a balanced perspective on clinical applications for women facing immune-related causes of RPL. [ABSTRACT FROM AUTHOR]

The editorial in "Frontiers in Immunology" discusses the immune responses involved in the progression of allergy and asthma, focusing on Th2 cell response, IgE signaling, Tregs, oxidative stress, and epigenetic regulation. Studies highlighted in the editorial show how these immune mechanisms contribute to airway inflammation, bronchoconstriction, and chronic inflammation in allergic asthma. Researchers emphasize the need for targeted therapies to regulate Th2 cytokines, enhance Treg function, and target oxidative stress and epigenetic mechanisms to improve clinical outcomes for asthma and allergic diseases. The development of personalized treatments based on individual immunological profiles may offer new avenues for more effective management of these conditions. [Extracted from the article]

The topic of ragweed pollen (RW) versus house dust mites (HDMs) has often been deliberated, but the increasing incidence of co-sensitization between them has been scarcely addressed. Utilizing Sprague Dawley rats, we explored the effects of co-sensitization with the combination of HDMs and RW pollen extracts in correlation with high-fructose diet (HFrD) by in vitro tracheal reactivity analysis in isolated organ bath and biological explorations. Our findings unveiled interrelated connections between allergic asthma, dyslipidemia, and HFrD-induced obesity, shedding light on their compounding role through inflammation. The increased CRP values and airway hyperresponsiveness to the methacholine challenge suggest a synergistic effect of obesity on amplifying the existing inflammation induced by asthma. One of the major outcomes is that the co-sensitization to HDMs and RW pollen led to the development of a severe allergic asthma phenotype in rats, especially in those with HFrD. Therefore, the co-sensitization to these allergens as well as the HFrD may play a crucial role in the modulation of systemic inflammation, obesity, and airway reactivity. [ABSTRACT FROM AUTHOR]

Pollen from common ragweed is an important allergen source worldwide and especially in western and southern Romania. More than 100 million patients suffer from symptoms of respiratory allergy (e.g., rhinitis, asthma) to ragweed pollen. Among the eleven characterized allergens, Amb a 6 is a non-specific lipid transfer protein (nsLTP). nsLTPs are structurally stable proteins in pollen and food from different unrelated plants capable of inducing severe reactions. The goal of this study was to produce Amb a 6 as a recombinant and structurally folded protein (rAmb a 6) and to characterize its physicochemical and immunological features. rAmb a 6 was expressed in Spodoptera frugiperda Sf9 cells as a secreted protein and characterized by mass spectrometry and circular dichroism (CD) spectroscopy regarding molecular mass and fold, respectively. The IgE-binding frequency towards the purified protein was evaluated using sera from 150 clinically well-characterized ragweed-allergic patients. The allergenic activities of rAmb a 6 and the nsLTP from the weed Parietaria judaica (Par j 2) were evaluated in basophil activation assays. rAmb a 6-specific IgE reactivity was associated with clinical features. Pure rAmb a 6 was obtained by insect cell expression. Its deduced molecular weight corresponded to that determined by mass spectrometry (i.e., 10,963 Da). rAmb a 6 formed oligomers as determined by SDS-PAGE under non-reducing conditions. According to multiple sequence comparisons, Amb a 6 was a distinct nsLTP with less than 40% sequence identity to currently known plant nsLTP allergens, except for nsLTP from Helianthus (i.e., 52%). rAmb a 6 is an important ragweed allergen recognized by 30% of ragweed pollen allergic patients. For certain patients, rAmb a 6-specific IgE levels were higher than those specific for the major ragweed allergen Amb a 1 and analysis also showed a higher allergenic activity in the basophil activation test. rAmb a 6-positive patients suffered mainly from respiratory symptoms. The assumption that Amb a 6 is a source-specific ragweed allergen is supported by the finding that none of the patients showing rAmb a 6-induced basophil activation reacted with Par j 2 and only one rAmb a 6-sensitized patient had a history of plant food allergy. Immunization of rabbits with rAmb a 6 induced IgG antibodies which strongly inhibited IgE binding to rAmb a 6. Our results demonstrate that Amb a 6 is an important source-specific ragweed pollen allergen that should be considered for diagnosis and allergen-specific immunotherapy of ragweed pollen allergy. [ABSTRACT FROM AUTHOR]

Na+/K+ ATPase is a protein involved in the active transport of ions across the cellular membrane. Ouabain is a cardiotonic glycoside that, by inhibiting the Na+/K+ pump, interferes with cell processes mediated directly by the pump, but also indirectly influences other cellular processes such as cell cycle and proliferation, growth, cell differentiation, angiogenesis, migration, adhesion, and invasion. We used the SK-BR-3 breast cancer cell line, mesenchymal stem cells (MSCs), and tumor-associated fibroblasts (TAFs) in vitro to determine the effects of ouabain exposure on these cellular types. The results showed a multi-level effect of ouabain mainly on tumor cells, in a dose-dependent manner, while the TAFs and their normal counterparts were not significantly influenced. Following exposure to ouabain, the SK-BR-3 cells changed their morphologic appearance, decreased the expression of immunophenotypic markers (CD29, Her2, VEGF), the proliferation rate was significantly decreased (Ki67 index), the cells were blocked in the G0 phase of the cell cycle and suffered necrosis. These data were correlated with the variable expression of α and β Na+/K+ pump subunits in tumor cells, resulting in decreased ability to adhere to the VCAM-1 substrate in functional flow chamber studies. Being indicative of the pro-apoptotic and inhibitory effect of ouabain on tumor invasion and metastasis, the results support the addition of ouabain to the oncological therapeutic arsenal, trailing the "repurposing drugs" approach. [ABSTRACT FROM AUTHOR]

We present a comparative study of the plasticity of rat bone marrow mesenchymal stem cells (MSCs) and rat muscle-derived stem cells (MDSCs). The study was performed on two cell populations that were isolated by aspiration from the femur bone marrow and gastrocnemius muscle biopsy of 6-week-old albino rats. Both cell populations were exposed to identical stimulation conditions. The cells were capable of undergoing osteogenic, chondrogenic, adipogenic and epithelial differentiation, as shown by histochemistry and immunostaining techniques. The MDSC population showed behavior and characteristics similar to the bone marrow MSC population; however, the osteogenic and adipogenic potential was more reduced compared to MSCs. Our results indicate a positive expression of E cadherin and Cytokeratin 10 after 28 days under epithelial stimulation, suggesting a potential use for gastrocnemius muscle MDSCs as a promising source for regenerative therapies, including re-epithelialization and skin regeneration.

INTRODUCTION An increase of severe and complex phenotypes of allergy has been recently documented, especially in the young population and in children. Allergic rhinitis has a prevalence of up to 50% per selected age groups in certain countries. OBJECTIVES AND BACKGROUND This study aims to evaluate disease severity and life quality impairment in allergic patients. MATERIALS AND METHODS Allergic patients were evaluated in the Allergology Clinic. We selected a total number of 84 patients with seasonal pollinosis who lacked other respiratory comorbidities. An objective symptoms score was constructed and checked against patients’ self-evaluation score, both scores ranging on a scale of 1 to 10. RESULTS The most frequent clinical manifestations were nasal symptoms (mainly nasal obstruction and rhinorrhea in almost 80% of patients), as well as ocular symptoms (mainly pruritus in 65% of patients). We found a moderate correlation (rho=0.508, p

Allergic asthma is a chronic airway inflammatory disorder triggered by inhalant allergens. Interleukin (IL)-4 and IL-13 play a main role in the generation of T helper cell type 2 (Th2) immune response, induction of immunoglobulin E (IgE) synthesis and persistence of airway inflammation. The aim of the present study was to investigate the influence of Dermatophagoides pteronyssinus allergen Der p 1, the major allergen of house dust mite, on the synthesis of IL-4 and IL-13 by monocyte-derived dendritic cells (DCs) and naive CD4 + T cells cocultured with DCs, as well as their role in the production of serum IgE, in house dust mite (HDM) allergic patients. Peripheral blood mononuclear cells (PBMCs) were isolated from venous blood of patients allergic to HDM and healthy donors and incubated with granulocyte-macrophage colony-stimulating factor (GM-CSF) and IL-4 to generate immature DCs. The obtained cells were stimulated for 24 h with Der p 1 to induce DC maturation, washed, and afterwards cocultured for 24 h with autologous naive CD4 + T cells. Culture supernatants were harvested for IL-4, IL-13 and IFN-γ level measurements. DCs stimulation with Der p 1 induced higher synthesis of IL-4 and IL-13 in HDM allergic patients, compared to healthy donors. The allergic group showed significant correlation between IL-13 production by Der p 1-pulsed DCs, and total serum IgE and IL-4 production of the same cells and Der p-specific IgE. To conclude, IL-4 and IL-13 are critically related to the regulation of serum IgE production in patients with allergic asthma. The relevance of these two cytokines in the pathophysiology of Th2 asthma endotype makes them an appropriate target in its management., (Copyright: © Cernescu et al.)