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Respiratory Illnesses Caused by Diesel Fuel Exhaust Emissions
Published in Ozcan Konur, Petrodiesel Fuels, 2021
Li et al. (2004) study the mechanism by which redox cycling organic chemicals, prepared from DEP, induce phase II enzyme expression as a protective response in a paper with 327 citations. They showed that aromatic and polar DEP fractions, which are enriched in PAHs and quinones, respectively, induce the expression of ‘heme oxygenase-1’ (HO-1), GST, and other phase II enzymes in macrophages and epithelial cells. They then showed that HO-1 expression is mediated through accumulation of the bZIP transcription factor, NRF2, in the nucleus, and that NRF2 gene targeting significantly weakens this response. NRF2 accumulation and subsequent activation of the antioxidant response element is regulated by the proteasomal degradation of NRF2. This pathway is sensitive to pro-oxidative and electrophilic DEP chemicals and is also activated by ambient ultrafine particles. They propose that NRF2-mediated phase II enzyme expression protects against the proinflammatory effects of particulate pollutants in the setting of allergic inflammation and asthma.
Epidemiology of Microbiological Contamination of Indoor Environments
Published in Rafał L. Górny, Microbiological Corrosion of Buildings, 2020
Microorganisms colonising water-damaged buildings play an important role in the pathogenesis of many allergic diseases, including asthma, allergic alveolitis, allergic rhinitis, allergic conjunctivitis and sinusitis, allergic inflammation of the nasal mucosa, sarcoidosis and allergic bronchopulmonary aspergillosis. Allergic reactions to moulds are quite common and can affect about 20% of the world’s population (3–10% in Europe). The most allergenic fungi include those of Alternaria, Aspergillus, Cladosporium, Mucor, Penicillium and Trichoderma genera [Górny and Dutkiewicz 2002; Denning et al. 2014; Kurup et al. 2002; Hurraß et al. 2017]. Hypersensitivity to fungal allergens is a significant risk factor for the development of severe bronchial asthma. It is estimated that, among 22 million people with asthma, about 5 million cases are caused by poor living conditions, in particular increased humidity and associated exposure to moulds [Mudarri and Fisk 2007]. According to the ‘Healthy Homes Barometer 2017’ report, about 2.2 million Europeans suffer from asthma caused by their living conditions [Rasmussen et al. 2017].
Will Systems Biology Transform Clinical Decision Support?
Published in Paul Cerrato, John Halamka, Reinventing Clinical Decision Support, 2020
Transcriptome. Advances in transcriptomics are likewise providing insights into the pathophysiology of asthma. The transcriptome refers to RNA strands in our cells. Body proteins that carry out essential biological functions are created through a 3-step process: DNA provides the basic building blocks—the genes. These genes then go through the process of transcription, in which they are “converted” into RNA, which in turn undergoes the process of translation, which results in the generation of body proteins, including enzymes. As Bunyavanich and Shadt explain, “Transcriptomics offers a complementary and synergistic approach to GWAS for studying disease, as RNA reflects the more dynamic processes at play in a given tissue or tissues that underlie pathophysiology.”18 RNA sequencing has identified gene transcripts linked to eosinophilic esophagitis, a form of allergic inflammation of the esophagus, which are consistent with GWAS of patients with eosinophilic esophagitis. The GWAS also reveal relevant genetic variants on chromosome 5 (5q22). Similarly, RNA sequencing of airway biopsies has found several specific expressed genes, including SLC26A4, POSTN, and BCL2.
Correlation between mast cell-mediated allergic inflammation and length of perfluorinated compounds
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Allergic inflammation is an abnormal reaction of the body evidenced as over-reaction of the immune system (Hainsworth 2003). Mast cells are known to play a key role in allergic inflammation, and release various inflammatory mediators, including histamine, cytokines, chemokines, and proteases (Amin 2012). Histamine is released by the degranulation of mast cells and is one of the predominant mediators leading to immediate-type hypersensitivity (Amin 2012). Mast cell degranulation is induced by calcium (Ca) mobilization through granule membrane fusion (Nishida et al. 2005). Subsequently, this induces activation of transcription factor nuclear factor (NF)-κB and release of inflammatory cytokines and chemokines (Liu et al. 2017). NF-κB regulates expression of pro-inflammatory cytokines and chemokines known to produce increased vascular permeability, inflammation, and tissue remodeling (Kempe et al. 2005).