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Physiology of the Airways
Published in Anthony J. Hickey, Sandro R.P. da Rocha, Pharmaceutical Inhalation Aerosol Technology, 2019
Anthony J. Hickey, David C. Thompson
Mast cells are located in the walls of the central and peripheral airways and may be found free in the lumen of the airways (Cutz and Orange, 1977). Activation by antigen cross-bridging of surface antibodies elicits cellular degranulation of the mast cell and the release of biologically active preformed and newly generated mediators. Also released are proteases, including chymase and tryptase, which can modify airway function by degrading biologically active proteins and peptides (Caughey, 1991). In addition, tryptase activates protease-activated receptors, leading a variety of unanticipated biological actions, such as induction of airway smooth muscle proliferation (Abraham, 2002; Cocks and Moffatt, 2001). Mast cells serve an important role in the response of the airways to challenge by antigens (or allergens).
Eosinophilic pneumonia induced by drugs
Published in Philippe Camus, Edward C Rosenow, Drug-induced and Iatrogenic Respiratory Disease, 2010
In drug-induced eosinophilic lung disease, antigen-presenting cells, such as alveolar macrophages and dendritic cells, consume drugs and then present them as antigens via their MHC receptors. This antigen–receptor complex is recognized by the Th2 lymphocyte T-cell receptor in conjunction with the lymphocyte CD4 receptor. This in turn activates the Th2 lymphocyte to release IL-5 and results in eosinophil production, chemotaxis to the lung, and degranulation (Fig. 23.2). The relative abundance of macrophages and dendritic cells in the lung could result in relatively large local production of IL-5 and eotaxin with the consequence of preferential accumulation of eosinophils within the lung.
Cardiovascular and Other Illnesses Caused by Diesel Fuel Exhaust Emissions
Published in Ozcan Konur, Petrodiesel Fuels, 2021
Nemmar et al. (2004b) study the relationship between airway inflammation and thrombosis 24 hours after intratracheal instillation of DEPs (50 μg/hamster) in a paper with 89 citations. They induced mild thrombosis in the femoral vein by endothelial injury and studied the consequences of airway inflammation on thrombogenicity via online video microscopy. They performed lung inflammation and histamine analysis in BAL and plasma after pretreatment with ‘dexamethasone’ (DEX) or ‘sodium cromoglycate’ (SC). They found that DEP-induced airway inflammation and histamine release in BAL and in plasma, and increased thrombosis, without elevating plasma von ‘Willebrand factor’ (vWF) levels. The IT instillation of 400 nm positively charged polystyrene particles (500 μg/hamster), serving as particles that do not penetrate into the circulation, equally produced airway inflammation, histamine release, and enhanced thrombosis. Histamine in plasma resulted from basophil activation. ‘Intraperitoneal’ (IP) pretreatment with DEX (5 mg/kg) abolished the DEP-induced histamine increase in BAL and plasma and abrogated airway inflammation and thrombogenicity. The IT pretreatment with DEX (0.5 mg/kg) showed a partial but parallel inhibition of all of these parameters. Pretreatment with SC (40 mg/kg, IP) strongly inhibited airway inflammation, thrombogenicity, and histamine release. Their results are compatible with the triggering of mast cell degranulation and histamine release by DEP. They conclude that histamine plays an initial central role in airway inflammation, further release of histamine by circulating basophils, and peripheral thrombotic events. Antiinflammatory pretreatment can abrogate the peripheral thrombogenicity by preventing histamine release from mast cells.
Short-term exposure of female BALB/cJ mice to e-cigarette aerosol promotes neutrophil recruitment and enhances neutrophil-platelet aggregation in pulmonary microvasculature
Published in Journal of Toxicology and Environmental Health, Part A, 2023
Hunter T. Snoderly, Hassan Alkhadrawi, Dhruvi M. Panchal, Kelly L. Weaver, Jenna N. Vito, Kasey A. Freshwater, Stell P. Santiago, I. Mark Olfert, Timothy R. Nurkiewicz, Margaret F. Bennewitz
Collectively, these results suggest that EC exposure mediates neutrophil recruitment to the lung vasculature but impairs their ability to traverse the blood-air barrier to effectively respond to respiratory insult. Supporting this, the reduced presence of MPO activity in plasma suggests neutrophil azurophilic degranulation was impaired two days post-exposure, thereby diminishing effectiveness of neutrophil antimicrobial activity. These findings aid in contextualizing why EC exposure appears to enhance susceptibility to bacterial and viral respiratory infections including pseudomonas aeruginosa, influenza, and COVID-19 (Corriden et al. 2020; Madison et al. 2020; Wang et al. 2020). Impaired degranulation, which may result in a decreased capacity for neutrophil response to bacterial insult, coupled with the observation that neutrophils appeared to build up and undergo pro-inflammatory interactions with platelets in the lung vasculature, might account for previous observations showing neutrophils undergo both pro-inflammatory and immunosuppressive changes following EC exposure. Alternatively, elevated MPO activity may have produced an apparently lower MPO activity if the ELISA failed to detect other forms of MPO in its enzymatic cycle, which primarily generate hypochlorous acid and hydrogen peroxide to aid in antimicrobial functionality or promote inflammation (Siraki 2021).
A comprehensive summary of disease variants implicated in metal allergy
Published in Journal of Toxicology and Environmental Health, Part B, 2022
Type I hypersensitivity responses are immediate-type allergic reactions mediated by antigen-specific immunoglobulin (Ig)E molecules. In sensitized individuals, B-cells produce these antibodies, which are then bound by FcεRI (high affinity IgE receptor) molecules expressed on granulocyte cell surfaces including mast cells and basophils. Antigen exposure facilitates IgE cross-linking, and subsequently, cellular degranulation (Murphy, Travers, and Walport 2012). Preformed molecular mediators, including histamine, tryptase, and various cytokines/chemokines, are released during this process and are responsible for the prototypical physiological alterations such as vasodilation or bronchoconstriction observed during this type of allergic response (Hausmann, Schnyder, and Pichler 2010; Moon, Befus, and Kulka 2014). Some examples of type I hypersensitivity responses include anaphylaxis, allergic asthma, allergic rhinitis, and contact urticaria.
Influence of o,p′-DDT on MUC5AC expression via regulation of NF-κB/AP-1 activation in human lung epithelial cells
Published in Journal of Toxicology and Environmental Health, Part A, 2021
Gi Ho Lee, Sun Woo Jin, Jae Ho Choi, Eun Hee Han, Yong Pil Hwang, Chul Yung Choi, Hye Gwang Jeong
Endocrine disruptors are postulated to play a prominent role in the etiology of airway inflammation. Several investigators reported that endocrine disruptors enhance airway hyper-responsiveness and allergic airway inflammation characterized by goblet cell hyperplasia and leukocyte infiltration in mice (Castaneda et al. 2017; Lee and Lawrence 2018; Loffredo, Coden, and Berdnikovs 2020; Yanagisawa et al. 2019). In addition, endocrine disruptors induced secretion of IgE and Th1/Th2 cytokines (Bornehag and Nanberg 2010; Kato et al. 2006; Kawano et al. 2012; Tajiki-Nishino et al. 2018). Although endocrine disruptors induced IgE-mediated mast cell degranulation and airway hyper-responsiveness, the effects on mechanisms underlying MUC5AC expression-related airway inflammation remain unclear. Data demonstrated that o,p′-DDT increased MUC5AC mRNA expression by promoting its transcription associated with stimulation of NF-κB and AP-1 signaling pathways in A549 cells. This is the first report showing that o,p′-DDT enhanced MUC5AC expression in vitro.