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.

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.

Emerging evidence suggests a critical role of the gut microbiome in modulating systemic immune responses, with increasing relevance in dermatological diseases. Chronic spontaneous urticaria (CSU), traditionally viewed as an isolated cutaneous disorder, is now recognized as a systemic immune condition involving complex interactions between innate and adaptive immunity, mast cell dysregulation, and non-IgE-mediated pathways. This review explores the gut–skin axis as a unifying concept linking intestinal dysbiosis to inflammatory skin diseases, including atopic dermatitis, psoriasis, rosacea, and acne. Special emphasis is placed on CSU, where altered gut microbial composition, characterized by reduced diversity, depletion of short-chain fatty acid-producing bacteria, and expansion of Proteobacteria, may contribute to increased intestinal permeability, systemic immune activation via toll-like receptors, and heightened mast cell sensitivity. We discuss findings from animal models demonstrating that gut microbiota modulation can attenuate mast cell hyperreactivity and reduce urticarial symptoms. In parallel, we examine clinical evidence supporting the potential role of probiotics, prebiotics, dietary interventions, and fecal microbiota transplantation as adjunctive strategies in CSU management. Despite promising findings, challenges remain in translating microbiome research into effective therapies due to interindividual variability, the complexity of host–microbiome interactions, and a lack of standardized protocols. Future research should focus on identifying predictive microbial patterns and developing personalized microbiome-targeted interventions. Understanding the bidirectional gut–skin relationship may open new therapeutic avenues beyond symptomatic treatment, positioning the microbiome as a novel target in CSU and related inflammatory dermatoses.

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.

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.

Background: Asthma and atherosclerosis frequently coexist in clinical populations and share convergent immunometabolic pathways amplified by gut microbial dysbiosis. We propose the gut–lung–vascular axis as a unifying mechanistic framework connecting epithelial and endothelial inflammation providing a foundation for understanding shared inflammatory mechanisms beyond tissue-specific disease boundaries. Methods: A targeted narrative review systematically appraised clinical, experimental and multi-omics studies published over the last five years to delineate microbiota-driven pathways relevant to asthma and atherosclerosis. Particular emphasis was placed on specific microbial taxa, metabolite profiles and immunometabolic networks that connect gut dysbiosis with respiratory and cardiovascular dysfunction. Results: Across human and experimental cohorts, dysbiosis marked by depletion of short-chain fatty acids (SCFAs) producing taxa (Faecalibacterium, Roseburia, Bacteroides) and enrichment of pathobionts (Proteobacteria, Haemophilus, Moraxella, Streptococcus) promotes epithelial and endothelial barrier dysfunction, amplifying Th2/Th17-skewed inflammation and endothelial injury. Key metabolites, including SCFAs, trimethylamine N-oxide (TMAO), secondary bile acids (BA), indole/tryptophan derivatives and lipopolysaccharides (LPS), serve as molecular connectors linking gut, airway and vascular inflammation. Microbial signatures and metabolomic patterns hold emerging diagnostic and therapeutic potential, and several drug classes (e.g., statins, corticosteroids, proton-pump inhibitors (PPIs)) further modulate host–microbiota interactions. Conclusions: Shared microbial taxa and metabolite signatures in asthma and atherosclerosis support microbiota-mediated immune dysregulation along the gut–lung–vascular axis as a common pathogenic framework. Microbial and metabolite profiling may enable improved risk stratification and precise, microbiota-targeted therapies. Integrating microbiome-informed diagnostics and personalized interventions could help reduce systemic inflammation and the burden of these overlapping inflammatory diseases.