Topic Review
Air Pollution Affects Placental DNA Methylation
The Developmental Origins of Health and Disease (DOHaD) concept postulates that in utero exposures influence fetal programming and health in later life. Throughout pregnancy, the placenta plays a central role in fetal programming; it regulates the in utero environment and acts as a gatekeeper for nutrient and waste exchange between the mother and the fetus. Maternal exposure to air pollution, including heavy metals, can reach the placenta, where they alter DNA methylation patterns, leading to changes in placental function and fetal reprogramming. In this entry, we explore the current knowledge on placental DNA methylation changes associated with prenatal air pollution (including heavy metals) exposure and highlight its effects on fetal development and disease susceptibility.
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  • 15 Nov 2021
Topic Review
Air pollution and Fuel Combustion
Air pollution is a precursor to many health issues such as difficulty breathing, asthma, lung and heart diseases, and cancer. 
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  • 11 Jan 2022
Topic Review
Air Pollution Induced Disorders
Air pollution is a heterogeneous mixture of various constituents resulting from the complex interaction of multiple emissions and chemical reactions. This mixture comprises solid particles and liquid droplets suspended in the air, i.e., PM2.5, that can include organic carbon (OC), elemental or black carbon (EC), nitrates, sulfates, and metals (e.g., iron, vanadium, nickel, copper, and manganese) as well as gases (e.g., ground level ozone (O3), carbon monoxide (CO), sulfur dioxide (SO2), oxides of nitrogen (NOx)) gaseous organic compounds (e.g., non-methane volatile organic compounds (VOCs), polycyclic aromatic hydrocarbons (PAHs) and polychlorinated biphenyls (PCBs)), bacterial endotoxins (mostly bound to solid particles or liquid aerosols). There are two possible ways by which air pollutants enter the CNS, either through direct transport of particles into the CNS or via systemic inflammation upon initial recruitment of immune cells in the lung tissue. Once in the organism, the adverse effects of fine particulates on the brain rely mainly on three mechanisms. First, they can induce the release of proinflammatory mediators leading to chronic respiratory and systemic inflammation, thereby affecting the BBB and ultimately triggering neural-immune interaction and resulting in increased production of ROS and chronic oxidative stress. Second, the particles can damage the BBB through the direct formation of ROS and thereby alter the permeability of the barrier. Third, there can be mechanical stimulation of specific mechano-receptors in pulmonary tissue leading to the lung arc reflex and sympathetic activation with the release of vasoconstrictors such as catecholamines. 
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  • 26 Oct 2020
Topic Review
Air Pollution on Human Microbial Community
A balanced microbiota composition is requisite for normal physiological functions of the human body. Several environmental factors such as air pollutants may perturb the human microbiota composition. It is noticeable that currently around 99% of the world’s population is breathing polluted air. Air pollution’s debilitating health impacts have been studied scrupulously, including in the human gut microbiota.
  • 737
  • 06 Dec 2022
Topic Review
Airborne Bacteria in Dairy Farms
The environmental quality of farms plays an important role in the food safety of the dairy industry because it may influence the microbial communities in milk. The microorganisms present in the different areas of a farm have an influence on this environmental quality, using the air as a vehicle of dissemination. However, the ability of this airborne microbial community to contaminate the milk, like the sources of origin of these microorganisms, has not been well studied in dairy farms until now. 
  • 531
  • 25 Jan 2022
Topic Review
AIRE Gene
autoimmune regulator
  • 391
  • 24 Dec 2020
Topic Review
Airsacculitis
Airsacculitis, also known as air sacculitis, aerosacculitis, air sac disease, air sac infection, air sac syndrome and simply sac disease, is a common inflammatory condition of air sacs that occurs in birds and is caused by various microbial (mostly bacterial) taxa. Having multiple different causative agents, the condition is widely distributed around the world. Since the disease is highly infectious it is especially dangerous for domesticated birds (poultry) bred on big farms. Occurrence of airsacculitis in big flocks can mean high economic loss, as infected poultry needs to be carefully observed, with all of the infected tissue disposed of and not used for human food. In severe cases of the disease whole infected bird carcasses need to be disposed. Usually the disease affects younger birds, aged between 6 and 12 weeks. The most characteristic sign of airsacculitis is an inflamed mucous membrane of bird air sacs, which swells and becomes red, with infected birds exhibiting different symptoms, such as coughing, lethargy, swelling of the neck, difficult breathing, appetite and weight loss etc. The same term is used for bacterial infection and subsequent inflammation of laryngeal air sacs in non-human primates.
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  • 25 Oct 2022
Topic Review
Airway Epithelium in Asthma Pathobiology
The features of allergic asthma are believed to be mediated mostly through the Th2 immune response. In this Th2-dominant concept, the airway epithelium is presented as the helpless victim of Th2 cytokines. Asthma researchers started believing in that the airway epithelium played a crucial role, as alarmins, which are the inducers of type 2 innate lymphoid cell (ILC2), are almost exclusively secreted by the airway epithelium. This underscores the eminence of airway epithelium in asthma pathogenesis. However, the airway epithelium has a bipartite functionality in sustaining healthy lung homeostasis and asthmatic lungs. On the one hand, the airway epithelium maintains lung homeostasis against environmental irritants/pollutants with the aid of its various armamentaria, including its chemosensory apparatus and detoxification system. Alternatively, it induces an ILC2-mediated type 2 immune response through alarmins to amplify the inflammatory response. However, the available evidence indicates that restoring epithelial health may attenuate asthmatic features.
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  • 16 Mar 2023
Topic Review
Airway Inflammation
The effects of airway inflammation on airway smooth muscle (ASM) are mediated by pro-inflammatory cytokines such as tumor necrosis factor alpha (TNFα).
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  • 12 Jan 2021
Topic Review
Airway Smooth Muscle Calcium Handling Mechanisms and Estrogens
Cell calcium (Ca2+) homeostasis is maintained by a finely tuned Ca2+ signaling system made-up of numerous Ca2+ transporters (channels, exchangers, and pumps) regulating the influx and efflux of this cation from the cytoplasm to preserve its balance. Ca2+ homeostasis is essential for the cell. As a second messenger, Ca2+ signaling regulates various cellular processes that depend on the Ca2+ concentration. It is well known that Ca2+ regulates exocytosis, contraction, protein phosphorylation, dephosphorylation, metabolism, gene transcription, fecundation, cell proliferation, and even apoptosis. In the ASM, Ca2+ homeostasis keeps intracellular basal Ca2+ concentrations (b[Ca2+]i) at around 100–150 nM, while Ca2+ concentrations in the intracellular stores and extracellular space are higher (5–10 mM and 2 mM, respectively) creating a large chemical gradient in favor of Ca2+ influx into the cytosol. In order to regulate [Ca2+]i, numerous proteins exist to facilitate the cellular influx and efflux of Ca2+. Among the calcium-handling proteins, the voltage-dependent Ca2+ channels (VDCCs), store-operated Ca2+ channels (SOCCs), receptor-operated Ca2+ channel (ROCCs), transient receptor potential channels (TRPs), and the Na+/Ca2+ exchanger in its reverse form (NCXREV) as influx mechanisms located in the cellular membrane can be included. On the other hand, the Na+/Ca2+ Exchanger (NCX) and the plasma membrane Ca2+ ATPase (PMCA) are efflux mechanisms located in the cellular membrane.
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  • 15 May 2023
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