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Scientific Rationale for the Use of Single Herb Remedies in Ayurveda
Published in D. Suresh Kumar, Ayurveda in the New Millennium, 2020
S. Ajayan, R. Ajith Kumar, Nirmal Narayanan
Histopathological studies clearly showed the protective effect of extract against toluene diisocyanate-induced asthma. The extract offered significant protection against histamine and acetylcholine aerosol-induced bronchospasm in guinea pigs. A significant decrease in total leukocyte and differential leukocyte count in the broncho-alveolar lavage fluid of the egg albumin-sensitized guinea pigs was observed after administration of the extract. Treatment with the extract for three days inhibited the hypersensitivity reaction. The extract dose dependently protected the mast cell disruption induced by p-Methoxy-N- methylphenethylamine. Alcohol extract of V. negundo therefore offers not only bronchodilation, but also decreases bronchial hyperreactivity, thereby providing protection against asthma (Patel et al. 2010).
Epithelial Function and Airway Responsiveness
Published in Alastair G. Stewart, AIRWAY WALL REMODELLING in ASTHMA, 2020
Roy G. Goldie, Janet M. H. Preuss
Airway epithelial cells express and produce several cytokines, including granulocyte/macrophage colony-stimulating factor (GM-CSF), interleukin (IL)-lα, IL-1β, IL-6, and IL-8.85–88 Exposure of human bronchial epithelial cell cultures to toluene diisocyanate resulted in a marked increase in the release of IL-1β and IL-6.86 In guinea pig isolated trachea, IL-1 reduced the relaxant effect of isoprenaline,89 although this is not always observed.90 Interestingly, cultured bronchial epithelial cells from asthmatic individuals released more GM-CSF than cells from nonasthmatic individuals, and they also expressed increased levels of mRNA for GM-CSF.91 Furthermore, the production of proinflammatory cytokines by the human airway epithelial cells is increased following infection with respiratory syncytial virus,92,93 a virus commonly associated with exacerbations of asthma in young children.94
Effect of Neutrophils on Airway Smooth Muscle Responsiveness
Published in Devendra K. Agrawal, Robert G. Townley, Inflammatory Cells and Mediators in Bronchial Asthma, 2020
Toluene diisocyanate (TDI), a reactive chemical used in industry, can cause airflow obstruction and increased airway responsiveness in man and experimental animals. Exposure of unanesthetized guinea pigs to TDI results in an airway neutrophil infiltrate that occurs in synchrony with the development of increased airway reactivity.65 Depletion of circulating leukocytes with hydroxyurea blocked TDI-induced increased airway reactivity. However, depletion of leukocytes with a different cytotoxic agent, cyclophosphamide, did not block the development of heightened airway reactivity.66,67 The mechanism by which hydroxyurea prevented the increased responsiveness is unknown, but the study of Thompson et al.66 draws attention to the problems in assigning causation when neutrophils are present in a temporal association with alterations in nonspecific reactivity and cautions against the otherwise tempting conclusions to be drawn from neutrophil depletion studies.51
Bisphenol A, TH17 cells, and allergy: A commentary
Published in Journal of Immunotoxicology, 2022
Ian Kimber, Nicole Woeffen, Kevin Sondenheimer
It has also been reported that oral exposure of adult mice to BPA resulted in enhanced airway inflammation following sensitization and challenge with toluene diisocyanate (Tajiki-Nishino et al. 2018). It was found that the top dose of BPA caused a significant increase in eosinophils in the bronchoalveolar lavage fluid (BALF) of mice challenged with toluene diisocyanate. There was, however, no significant increase in total levels of IgE immunoglobulin. Moreover, there were comparable increases in the levels in BALF of IL-4 and interferon (IFN)-γ; cytokines that have opposing effects on IgE antibody production. Employing a mouse model of allergic rhinitis to OVA, Wang et al. (2020) reported that BPA exposure resulted in increased nasal symptoms and elevated levels of anti-OVA IgE antibodies.
Protective effects of N-acetylcysteine on a chemical-induced murine model of asthma
Published in Journal of Asthma, 2021
Jiafu Song, Lihong Yao, Jiaxin Shi, Jiashu Li, Caiyun Xu
Toluene diisocyanate (TDI) is a highly reactive small molecular chemical that is widely used for polyurethane foam manufacturing, autobody painting and repair, plastics manufacturing, and home decoration. It is one of the leading causes of occupational asthma, accounting for 10–25% of all adult-onset asthma (1). It is estimated that as many as 5% of workers exposed to diisocyanates develop asthma that may continue for a lifetime even after the exposure is discontinued (2). TDI-induced asthma is characterized by hyperresponsiveness, inflammation, and remodeling of the airways, often associated with marked infiltration of neutrophils and slight infiltration of eosinophils into the airways, which are resistant to steroid treatment (3). Clinically, TDI-induced asthma shares similar manifestations with allergic asthma induced by high molecular weight allergens, illustrating common pathogenic processes.
Asthma and rhinitis in Greek furniture workers
Published in Journal of Asthma, 2021
Katerina Paraskevaidou, Konstantinos Porpodis, Theodoros Kontakiotis, Ioannis Kioumis, Dionisios Spyratos, Despina Papakosta
WRA is often underdiagnosed (5). However, 5–25% of new cases of adult onset asthma can be attributed to the workplace (5–7). In the furniture industry, many different tasks are prone to wood dust exposure and several hazardous chemicals are used in paints, polishes, and lacquers either as solvents or as stabilizers of paint (e.g. acid N-butyl ester, acid ethyl ester, 2-butanone, toluene, xylene, ethyl ethoxy propyl ester, 2,4/2,6-toluene diisocyanate, formaldehyde, hexane, methylene chloride). Particleboard and fiberboard recently used more frequently are wood products containing adhesives and resins (8,9), but according to the European Union standards regarding implicated health hazards they are considered as natural wood (10,11). Therefore, the furniture industry is considered as a high-risk work environment for the development of WRA and WRR. Various studies have mainly examined the health effects of one agent, either toluene diisocyanate or formaldehyde (12,13). But workers in furniture processing could have an increased risk of developing WRA due to many other implicated substances.