Search Results (45)

Background: Patients with mastocytosis may present with exacerbated respiratory symptoms and lung diseases resulting from mast cell mediator release. However, their prevalence and severity level remain under debate. The study aims to analyze the prevalence of respiratory symptoms and the usefulness of lung function tests like spirometry, diffusing capacity of the lung for carbon monoxide (DLCO), and high-resolution computed tomography (HRCT) of the chest in mastocytosis patients presenting with dyspnea, cough, and exercise intolerance. Methods: We included 104 patients with mastocytosis and 71 healthy controls. Data collection encompassed patient interview, clinical examination, spirometry, DLCO, and chest HRCT. Diagnosis of mastocytosis included bone marrow biopsies and serum tryptase measurements. Results: Compared to controls, patients with mastocytosis exhibited significantly lower values in FEV1/VC ratio, absolute DLCO/VA, predicted DLCO/VA, absolute DLCOcSB, and predicted DLCOcSB (p < 0.001). Commonly reported respiratory symptoms included dyspnea (36.5%), chest tightness (22.1%), and wheezing (9.6%). Airway obstruction was identified in 7.7% of patients; however, it appeared to be independent of the mastocytosis subtype. A decreased DLCO/VA ratio was observed in 4.8% of patients, but HRCT did not reveal any evidence of underlying lung disease. Conclusions: Mastocytosis appears to be a risk factor for the occurrence and exacerbation of respiratory symptoms. However, airway obstruction and impairment of the alveolar–capillary membrane seem to occur independently of the clinical subtype of mastocytosis. Additionally, the causal relationship between pulmonary involvement, mast cell infiltration of the alveolar–capillary membrane, and the systemic circulation of mast cell mediators remains unclear and requires further research. Full article

Male-factor infertility accounts for approxiamately half of all infertility cases globally, yet therapeutic options remain limited for individuals with no retrievable spermatozoa, such as those with non-obstructive azoospermia (NOA). In recent years, artificial gametogenesis has emerged as a promising avenue for fertility restoration, driven by advances in two complementary strategies: organotypic in vitro spermatogenesis (IVS), which aims to complete spermatogenesis ex vivo using native testicular tissue, and in vitro gametogenesis (IVG), which seeks to generate male gametes de novo from pluripotent or reprogrammed somatic stem cells. To evaluate the current landscape and future potential of these approaches, a narrative, semi-systematic literature search was conducted in PubMed and Scopus for the period January 2010 to February 2025. Additionally, landmark studies published prior to 2010 that contributed foundational knowledge in spermatogenesis and testicular tissue modeling were reviewed to provide historical context. This narrative review synthesizes multidisciplinary evidence from cell biology, tissue engineering, and translational medicine to benchmark IVS and IVG technologies against species-specific developmental milestones, ranging from rodent models to non-human primates and emerging human systems. Key challenges—such as the reconstitution of the blood–testis barrier, stage-specific endocrine signaling, and epigenetic reprogramming—are discussed alongside critical performance metrics of various platforms, including air–liquid interface slice cultures, three-dimensional organoids, microfluidic “testis-on-chip” devices, and stem cell-derived gametogenic protocols. Particular attention is given to clinical applicability in contexts such as NOA, oncofertility preservation in prepubertal patients, genetic syndromes, and reprocutive scenarios involving same-sex or unpartnered individuals. Safety, regulatory, and ethical considerations are critically appraised, and a translational framework is outlined that emphasizes biomimetic scaffold design, multi-omics-guided media optimization, and rigorous genomic and epigenomic quality control. While the generation of functionally mature sperm in vitro remains unachieved, converging progress in animal models and early human systems suggests that clinically revelant IVS and IVG applications are approaching feasibility, offering a paradigm shift in reproductive medicine. Full article

The development of alternatives to animal models and traditional cell cultures has led to the emergence of organ-on-chip (OoC) systems, which replicate organ functions under both physiological and pathological conditions. These microfluidic platforms simulate key tissue interfaces—such as tissue–air, tissue–liquid, and tissue–tissue interactions—while incorporating biomechanical stimuli to closely resemble in vivo environments. This makes OoC systems particularly suitable for modeling biological barriers such as the skin, the placenta, and the blood–brain barrier, which play essential roles in maintaining homeostasis. This review explores various biological barrier models that can be replicated using the OoC technology, discussing the integration of induced pluripotent stem cells (iPSCs) to advance personalized medicine. Additionally, we examine the methods for assessing barrier formation, including real-time monitoring through integrated sensors, and discuss the advantages and challenges associated with these technologies. The potential of OoC systems in disease modeling, drug discovery, and personalized therapeutic strategies is also highlighted. Full article

Air pollution is a major global health threat, responsible for over 8 million deaths in 2021, including 700,000 fatalities among children under the age of five. It is currently the second leading risk factor for mortality worldwide. Key pollutants, such as particulate matter (PM_2.5, PM₁₀), ozone, sulfur dioxide, nitrogen oxides, and carbon monoxide, have significant adverse effects on human health, contributing to respiratory and cardiovascular diseases, as well as neurodevelopmental and neurodegenerative disorders. Among these, particulate matter poses the most significant threat due to its highly complex mixture of organic and inorganic compounds with diverse sizes, compositions, and origins. Additionally, it can penetrate deeply into tissues and cross the blood–brain barrier, causing neurotoxicity which contributes to the development of neurodegenerative diseases. Although the link between air pollution and neurological disorders is well documented, the precise mechanisms and their sequence remain unclear. Beyond causing oxidative stress, inflammation, and excitotoxicity, studies suggest that air pollution induces epigenetic changes. These epigenetic alterations may affect the expression of genes involved in stress responses, neuroprotection, and synaptic plasticity. Understanding the relationship between neurological disorders and epigenetic changes induced by specific air pollutants could aid in the early detection and monitoring of central nervous system diseases. Full article

Air pollution has well-documented adverse effects on human health; however, its impact on neurological diseases remains underrecognized. The mechanisms by which various components of air pollutants contribute to neurological disorders are not yet fully understood. This review focuses on key air pollutants, including particulate matter (PM_2.5 and PM₁₀), nitrogen dioxide (NO₂), ozone (O₃), carbon monoxide (CO), and diesel exhaust particles (DEPs). This paper summarizes key findings on the effects of air pollution on neurological disorders, including autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD), Alzheimer’s disease (AD), and Parkinson’s disease (PD). Although the precise biological mechanisms remain to be fully elucidated, evidence suggests that multiple pathways are involved, including blood–brain barrier disruption, oxidative stress, inflammation, and the activation of microglia and astrocytes. This review underscores the role of environmental pollutants as significant risk factors for various neurological diseases and explores their mechanisms of action. By advancing our understanding of these interactions, this work aims to inform new insights for mitigating the adverse effects of air pollution on neurological diseases, ultimately contributing to the establishment of a cleaner and healthier environment for future generations. Full article

Microplastics (MPs), defined as plastic particles smaller than 5 mm, have emerged as a global environmental and public health crisis, infiltrating air, water, soil, and food systems worldwide. MPs originate from the breakdown of larger plastic debris, single-use plastics, and industrial processes, entering food. Emerging evidence underscores the ability of MPs to cross biological barriers, including the blood–brain barrier, triggering neuroinflammatory responses and contributing to neurodegenerative diseases such as Alzheimer’s and Parkinson’s. Polystyrene (PS), a common type of MP, activates microglial cells, releasing pro-inflammatory cytokines like tumor necrosis factor (TNF-α) and interleukins, which increase neuronal damage. MPs have also been linked to cardiovascular diseases, with studies detecting polyethylene (PE) and polyvinyl chloride (PVC) in carotid artery plaques, increasing the risk of myocardial infarction and stroke. Furthermore, MPs disrupt endocrine function, alter lipid metabolism, and induce gut microbiome imbalances, posing multifaceted health risks. In the MENA region, MP pollution is particularly severe, with the Mediterranean Sea receiving an estimated 570,000 tons of plastic annually, equivalent to 33,800 plastic bottles per minute. Studies in Egypt, Lebanon, and Tunisia document high MP concentrations in marine ecosystems, with herbivorous fish like Siganus rivulatus containing over 1000 MPs per individual due to the ingestion of contaminated seaweed. Despite these findings, public awareness and regulatory frameworks remain inadequate, with only 24% of Egyptians demonstrating sufficient knowledge of safe plastic use. This review emphasizes the urgent need for region-specific research, policy interventions, and public awareness campaigns to address MP pollution. Recommendations include sustainable waste management practices, the promotion of biodegradable alternatives, and enhanced monitoring systems to mitigate the health and environmental impacts of MPs in the MENA region. Full article

Micro- and nano-plastics (MNPs) are small plastic particles that result from the breakdown of larger plastics. They are widely dispersed in the environment and pose a threat to wildlife and humans. MNPs are present in almost all everyday items, including food, drinks, and household products. Air inhalation can also lead to exposure to MNPs. Research in animals indicates that once MNPs are absorbed, they can spread to various organs, including the liver, spleen, heart, lungs, thymus, reproductive organs, kidneys, and even the brain by crossing the blood–brain barrier. Furthermore, MPs can transport persistent organic pollutants or heavy metals from invertebrates to higher levels in the food chain. When ingested, the additives and monomers that comprise MNPs can disrupt essential biological processes in the human body, thereby leading to disturbances in the endocrine and immune systems. During the 2019 coronavirus (COVID-19) pandemic, there was a significant increase in the global use of polypropylene-based face masks, leading to insufficient waste management and exacerbating plastic pollution. This review examines the existing research on the impact of MNP inhalation on human lung and kidney health based on in vitro and in vivo studies. Over the past decades, a wide range of studies suggest that MNPs can impact both lung and kidney tissues under both healthy and diseased conditions. Therefore, this review emphasizes the need for additional studies employing multi-approach analyses of various associated biomarkers and mechanisms to gain a comprehensive and precise understanding of the impact of MNPs on human health. Full article

Particulate matter (PM) negatively impacts brain health, while exercise training can mitigate these effects and promote brain health. However, the effect of the interaction between PM exposure and exercise on brain health remains insufficiently explored. This study investigated the effects of PM exposure and exercise training on neuroplasticity-related growth factors and blood–brain barrier (BBB) integrity. Forty male C57BL/6 mice were randomly assigned to four groups as follows: control (CON, n = 10), PM exposure (PM, n = 10), exercise training (EX, n = 10), and PM exposure with exercise training (PMEX, n = 10). PM exposure and exercise training interventions were conducted over 8 weeks. The PM group showed significantly elevated levels of malondialdehyde (MDA), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), S100 calcium-binding protein β (S100β), and neuron-specific enolase (NSE) (p < 0.05) and reduced levels of superoxide dismutase (SOD), insulin-like growth factor-1 (IGF-1), brain-derived neurotrophic factor (BDNF), and vascular endothelial growth factor (VEGF) (p < 0.05) compared to the CON and EX groups. Conversely, the EX group demonstrated significantly reduced MDA, IL-6, TNF-α, S100β, and NSE levels (p < 0.05) and enhanced SOD, IGF-1, BDNF, and VEGF levels (p < 0.05) compared to the PM group. However, the PMEX group exhibited attenuated benefits, showing higher MDA, IL-6, TNF-α, S100β, and NSE levels (p < 0.05) and lower SOD and IGF-1 levels (p < 0.05) compared to the EX group. These findings suggest that PM exposure induces oxidative stress, inflammation, and BBB disruption while downregulating neuroplasticity-related growth factors. Exercise training mitigates these adverse effects by enhancing antioxidant activity, reducing inflammation, upregulating neuroplasticity-related growth factors, and preserving BBB integrity. However, the protective effects of exercise may be partially diminished under conditions of PM exposure. Full article

Endocrine-disrupting chemicals (EDCs) are a growing health hazard for humankind and respiratory health in particular. Such chemical compounds are present in the environment and food and may interfere with physiological processes through interference with functions of the endocrine system, making humans more susceptible to various types of diseases. This review aims to discuss the effects of EDCs on the respiratory system. Exposure to EDCs during fetal development and adulthood increases susceptibility to respiratory diseases such as asthma, COPD, and pulmonary fibrosis. EDCs are both multiple and complex in the ways they can act. Indeed, these chemicals may induce oxidative stress, modify cell proliferation and differentiation, interfere with tissue repair, and modulate the inflammatory response. Moreover, EDCs may also break the integrity of the blood–air barrier, allowing noxious substances to penetrate into the lung and thus enhancing the opportunity for infection. In conclusion, the scientific evidence available tends to indicate that EDCs exposure is strongly linked to the initiation of respiratory disease. Further research will be important in discovering the underlying molecular mechanisms and devising preventive and therapeutic measures. Full article

Military burn pits, used for waste disposal in combat zones, involve the open-air burning of waste materials, including plastics, metals, chemicals, and medical waste. The pits release a complex mixture of occupational toxic substances, including particulate matter (PM), volatile organic compounds (VOCs), heavy metals, dioxins, and polycyclic aromatic hydrocarbons (PAHs). Air pollution significantly impacts brain health through mechanisms involving neuroinflammation. Pollutants penetrate the respiratory system, enter the bloodstream, and cross the blood–brain barrier (BBB), triggering inflammatory responses in the central nervous system (CNS). Chronic environmental exposures result in sustained inflammation, oxidative stress, and neuronal damage, contributing to neurodegenerative diseases and cognitive impairment. Veterans exposed to burn pit toxins are particularly at risk, reporting higher rates of respiratory issues, neurological conditions, cognitive impairments, and mental health disorders. Studies demonstrate that Veterans exposed to these toxins have higher rates of neuroinflammatory markers, accelerated cognitive decline, and increased risks of neurodegenerative diseases. This narrative review synthesizes the research linking airborne pollutants such as PM, VOCs, and heavy metals to neuroinflammatory processes and cognitive effects. There is a need for targeted interventions to mitigate the harmful and escalating effects of environmental air pollution exposures on the CNS, improving public health outcomes for vulnerable populations, especially for Veterans exposed to military burn pit toxins. Full article

Air pollution, a growing concern for public health, has been linked to various respiratory and cardiovascular diseases. Emerging evidence also suggests a link between exposure to air pollutants and neurodegenerative diseases, particularly Alzheimer’s disease (AD). This review explores the composition and sources of air pollutants, including particulate matter, gases, persistent organic pollutants, and heavy metals. The pathophysiology of AD is briefly discussed, highlighting the role of beta-amyloid plaques, neurofibrillary tangles, and genetic factors. This article also examines how air pollutants reach the brain and exert their detrimental effects, delving into the neurotoxicity of air pollutants. The molecular mechanisms linking air pollution to neurodegeneration are explored in detail, focusing on oxidative stress, neuroinflammation, and protein aggregation. Preclinical studies, including in vitro experiments and animal models, provide evidence for the direct effects of pollutants on neuronal cells, glial cells, and the blood–brain barrier. Epidemiological studies have reported associations between exposure to air pollution and an increased risk of AD and cognitive decline. The growing body of evidence supporting air pollution as a modifiable risk factor for AD underscores the importance of considering environmental factors in the etiology and progression of neurodegenerative diseases, in the face of worsening global air quality. Full article

Arsenic (As) is a metalloid naturally present in the environment, in food, water, soil, and air; however, its chronic exposure, even with low doses, represents a public health concern. For a long time, As was used as a pigment, pesticide, wood preservative, and for medical applications; its industrial use has recently decreased or has been discontinued due to its toxicity. Due to its versatile applications and distribution, there is a wide spectrum of human As exposure sources, mainly contaminated drinking water. The fact that As is present in drinking water implies chronic human exposure to this metalloid; it has become a worldwide health problem, since over 200 million people live where As levels exceed safe ranges. Many health problems have been associated with As chronic exposure including cancer, cardiovascular diseases, gastrointestinal disturbances, and brain dysfunctions. Because As can cross the blood–brain barrier (BBB), the brain represents a target organ where this metalloid can exert its long-term toxic effects. Many mechanisms of As neurotoxicity have been described: oxidative stress, inflammation, DNA damage, and mitochondrial dysfunction; all of them can converge, thus leading to impaired cellular functions, cell death, and in consequence, long-term detrimental effects. Here, we provide a current overview of As toxicity and integrated the global mechanisms involved in cognitive and behavioral impairment induced by As exposure show experimental strategies against its neurotoxicity. Full article

Environmental pollution of megacities can cause early biological damage such as DNA strand breaks and micronuclei formation. Comet assay tail length (TL) reflects exposure in the uterus to high levels of air pollution, primarily ozone and air particles (PM₁₀), including mothers’ smoking habits during pregnancy, conditions which can lead to low birth weight. In this biomonitoring study, we evaluated basal DNA damage in the cord blood cells of newborn children from Mexico City. We found a correlation between DNA damage in mothers and their newborns, including various parameters of environmental exposure and complications during pregnancy, particularly respiratory difficulties, malformations, obstetric trauma, neuropathies, and nutritional deficiencies. Mothers living in the southern part of the city showed double DNA damage compared to those living in the northern part (TL 8.64 μm vs. 4.18 μm, p < 0.05). Additionally, mothers’ DNA damage correlates with exposure to NOx (range 0.77–1.52 ppm) and PM₁₀ (range 58.32–75.89 μg/m³), as well maternal age >29. These results highlight the sensitivity of the comet assay in identifying differential in utero exposure for newborns whose mothers were exposed during pregnancy. They also suggest the importance of antioxidants during pregnancy and the role of the placental barrier in protecting the newborn from the DNA-damaging effects of oxidative pollution. Full article

Chronic rhinosinusitis (CRS) with (CRSwNP) or without (CRSsNP) nasal polyps is a prevalent and heterogeneous disorder existing as a spectrum of clinical conditions with complex underlying pathomechanisms. CRS comprises a broad syndrome characterized by multiple immunological features involving complex interactions between the genes, the microbiome, host- and microbiota-derived exosomes, the epithelial barrier, and environmental and micromilieu exposures. The main pathophysiological feature is an epithelial barrier disruption, accompanied by microbiome alterations and unpredictable and multifactorial immunologic overreactions. Extrinsic pathogens and irritants interact with multiple epithelial receptors, which show distinct expression patterns, activate numerous signaling pathways, and lead to diverse antipathogen responses. CRSsNP is mainly characterized by fibrosis and mild inflammation and is often associated with Th1 or Th17 immunological profiles. CRSwNP appears to be associated with moderate or severe type 2 (T2) or Th2 eosinophilic inflammation. The diagnosis is based on clinical, endoscopic, and imaging findings. Possible CRS biomarkers from the peripheral blood, nasal secretions, tissue biopsies, and nasally exhaled air are studied to subgroup different CRS endotypes. The primary goal of CRS management is to maintain clinical control by nasal douching with isotonic or hypertonic saline solutions, administration of nasal and systemic steroids, antibiotics, biologic agents, or, in persistent and more severe cases, appropriate surgical procedures. Full article

The lung promptly responds to edemagenic conditions through functional adaptations that contrast the increase in microvascular filtration. This review presents evidence for early signaling transduction by endothelial lung cells in two experimental animal models of edema, hypoxia exposure, and fluid overload (hydraulic edema). The potential role of specialized sites of the plasma membranes considered mobile signaling platforms, referred to as membrane rafts, that include caveolae and lipid rafts, is presented. The hypothesis is put forward that early changes in the lipid composition of the bilayer of the plasma membrane might trigger the signal transduction process when facing changes in the pericellular microenvironment caused by edema. Evidence is provided that for an increase in the extravascular lung water volume not exceeding 10%, changes in the composition of the plasma membrane of endothelial cells are evoked in response to mechanical stimuli from the interstitial compartment as well as chemical stimuli relating with changes in the concentration of the disassembled portions of structural macromolecules. In hypoxia, thinning of endothelial cells, a decrease in caveolae and AQP-1, and an increase in lipid rafts are observed. The interpretation of this response is that it favors oxygen diffusion and hinder trans-cellular water fluxes. In hydraulic edema, which generates greater capillary water leakages, an increase in cell volume and opposite changes in membrane rafts were observed; further, the remarkable increase in caveolae suggests a potential abluminal–luminal vesicular-dependent fluid reabsorption. Full article