Irritable bowel syndrome (IBS) is a common disease often considered as a functional intestinal disorder. Inflammation in IBS is a quite intriguing theory. The aim of this study was to investigate tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 expression in inflammatory bowel disease (IBD) patients, IBS patients and normal controls. IBS and IBD patients along with normal controls were recruited in the study. In all groups, 2 pinch biopsies were taken at each of 3 anatomical sites (terminal ileum, cecum, and rectum). IBS patients were also subcategorized according to the syndrome clinical manifestations. Two monoclonal antibodies (mAb), TNF-α mAb and IL-6 mAb, and one polyclonal antibody IL-1β mAb were applied for immunohistochemical analysis. In IBD patients intensity of TNF-α and IL-1β were lower than in IBS patients or controls, while IL-6 was significantly increased comparing to the aforementioned groups. In IBS patients TNF-α was increased comparing to IBD patients or controls, while IL-6 and IL-1β were similar to controls. In IBS subgroups, TNF-α was lower in diarrhea predominant IBS patients and higher constipation predominant IBS patients. Differences among IBS subgroups regarding IL-6 and IL-1β were nonsignificant. IL-6 seems to be the most important proinflammatory cytokine in IBD patients, while TNF-α could play a more significant role in IBS pathogenesis.

Severe pediatric asthma remains a significant clinical challenge despite advances in conventional therapy. Some children continue to experience persistent symptoms, recurrent exacerbations, and substantial morbidity despite optimized treatment with inhaled corticosteroids and long-acting bronchodilators. Advances in the understanding of asthma immunopathology, particularly type 2 (T2) inflammation, have led to the development of targeted biologics that modulate key inflammatory pathways. Several monoclonal antibodies are now approved for pediatric use, including the anti-immunoglobulin E (IgE) agent omalizumab, anti-interleukin (IL)-5 therapies such as mepolizumab, and the IL-4 receptor antagonist dupilumab. These biologics significantly reduce exacerbation rates, improve lung function, and decrease dependence on systemic corticosteroids in selected pediatric populations. Their effective use, however, requires careful assessment of clinical phenotypes and biomarkers, including blood eosinophils, serum IgE, and fractional exhaled nitric oxide. Uncertainties remain regarding treatment sequencing, duration, long-term safety, and cost-effectiveness. Agents targeting upstream epithelial cytokines, including tezepelumab, are broadening the therapeutic landscape. Despite this progress, pediatric evidence remains fragmented across age groups, biologic agents, study designs, and real-world cohorts, while many reviews focus on individual therapies or partly extrapolate from adult data. This review synthesizes pediatric evidence on efficacy, safety, biomarker-guided selection, age-related indications, and implementation challenges across approved and emerging biologics. It aims to provide clinicians with a practical framework for treatment selection and monitoring while identifying priorities for future pediatric research.

Allergic diseases are increasing globally, particularly among children, who are highly vulnerable due to critical windows of immune development. This review examines climate change as a key environmental determinant driving the rising burden of pediatric allergic diseases, including asthma, allergic rhinitis (AR), atopic dermatitis (AD), and food allergy (FA). Climate change influences disease risk through interconnected pathways, such as increased air pollution, altered aeroallergen patterns, and more frequent extreme weather events. Elevated carbon dioxide (CO₂) levels and rising temperatures prolong pollen seasons and enhance allergenicity, while pollutants such as ozone (O₃) and particulate matter (PM) exacerbate airway inflammation and immune dysregulation. Emerging evidence emphasizes the role of early-life exposure, particularly during prenatal and early postnatal periods, when environmental insults can induce long-term effects via epigenetic modifications and immune reprogramming. These mechanisms may increase susceptibility to allergic sensitization and subsequent disease development. Epidemiological studies consistently link exposure to air pollution, including PM₂.₅ (PM with aerodynamic diameter < 2.5 μm) and nitrogen dioxide (NO₂), with increased risk of allergic diseases in children. Additionally, climate change-related events such as wildfires, sand and dust storms, and thunderstorms further elevate exposure to allergens and pollutants, contributing to acute exacerbations and disease progression. Addressing this growing public health challenge requires integrated mitigation strategies to reduce greenhouse gas (GHG) emissions and improve air quality, alongside adaptive interventions to enhance resilience and reduce exposure. Understanding these mechanisms is essential for developing targeted prevention strategies and protecting child health in a changing climate.

Allergic diseases are increasing globally, particularly among children, who are highly vulnerable due to critical windows of immune development. This review examines climate change as a key environmental determinant driving the rising burden of pediatric allergic diseases, including asthma, allergic rhinitis (AR), atopic dermatitis (AD), and food allergy (FA). Climate change influences disease risk through interconnected pathways, such as increased air pollution, altered aeroallergen patterns, and more frequent extreme weather events. Elevated carbon dioxide (CO₂) levels and rising temperatures prolong pollen seasons and enhance allergenicity, while pollutants such as ozone (O₃) and particulate matter (PM) exacerbate airway inflammation and immune dysregulation. Emerging evidence emphasizes the role of early-life exposure, particularly during prenatal and early postnatal periods, when environmental insults can induce long-term effects via epigenetic modifications and immune reprogramming. These mechanisms may increase susceptibility to allergic sensitization and subsequent disease development. Epidemiological studies consistently link exposure to air pollution, including PM_2.5 (PM with aerodynamic diameter < 2.5 μm) and nitrogen dioxide (NO₂), with increased risk of allergic diseases in children. Additionally, climate change-related events such as wildfires, sand and dust storms, and thunderstorms further elevate exposure to allergens and pollutants, contributing to acute exacerbations and disease progression. Climate change may also contribute to allergic diseases through microbiome dysbiosis, as altered environmental microbial exposures, biodiversity loss, air pollution, and antibiotic-associated microbial disruption may impair immune tolerance and promote allergic sensitization in children. Addressing this growing public health challenge requires integrated mitigation strategies to reduce greenhouse gas (GHG) emissions and improve air quality, alongside adaptive interventions to enhance resilience and reduce exposure. Understanding these mechanisms is essential for developing targeted prevention strategies and protecting child health in a changing climate.

Background: Preschool wheezing is common, but distinguishing transient wheezing from early persistent asthma remains difficult. Oscillometric techniques, including impulse oscillometry (IOS), may provide objective prognostic information. Objective: To systematically review longitudinal studies assessing whether oscillometric measurements obtained at preschool age are associated with later asthma-related outcomes or lung function impairment. Methods: PubMed, Scopus, and MEDLINE (via EBSCOhost) were searched from inception to 28 February 2026. Eligible studies included preschool-aged children or closely related early-childhood populations assessed with IOS or forced oscillation technique (FOT), longitudinal follow-up, and later asthma-related or spirometric outcomes. Two reviewers independently screened studies, extracted data, and assessed risk of bias with QUIPS. Owing to substantial heterogeneity, findings were synthesized qualitatively. Results: Seven longitudinal cohort studies, encompassing 1077 children, met the eligibility criteria; baseline oscillometry was performed between ages 2 and 7 years, and follow-up ranged from 1 to 10 years. Short-term classification and longer-term prognostic studies were interpreted separately. Resistance-based indices, particularly R5, showed the most consistent associations with later asthma-related outcomes and lower subsequent spirometric indices, including FEV₁ and FEV_1/FVC. Most studies were at moderate risk of bias, and some reports came from related cohorts. Conclusions: Preschool oscillometry may provide complementary physiological information to assess asthma risk in symptomatic or high-risk preschool-aged children, particularly through resistance-based measures. However, evidence remains limited, heterogeneous, and insufficient to support a single validated cutoff, routine screening of apparently healthy children, or routine stand-alone prognostic use.

Hymenoptera stings in children are a recognized cause of severe and potentially fatal reactions, yet clinical attention has been predominantly focused on IgE-mediated anaphylaxis. This narrative review addresses the broader spectrum of non-IgE-mediated toxic and unusual reactions in the pediatric population, organized by affected organ system. Toxic envenomation—dose-dependent and independent of allergic sensitization—occurs when venom components directly disrupt cellular membranes, producing rhabdomyolysis, hemolysis, acute kidney injury, hepatotoxicity, ARDS, and multi-organ failure; a sting burden of ≥1 sting per kilogram body weight warrants urgent evaluation in children. Unusual non-IgE-mediated immunological reactions—including Guillain–Barré syndrome, ADEM, cavernous sinus thrombosis, Kounis syndrome, autoimmune thrombocytopenic purpura, and serum sickness—can be triggered by even a single sting and manifest days to weeks later. A clinically deceptive asymptomatic interval common to both categories frequently leads to premature discharge and delayed diagnosis. Awareness of this extended spectrum, weight-based hospitalization thresholds, and early organ-specific supportive care are essential to reduce preventable morbidity and mortality in this population.