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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 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]