File:Mechanisms of e-liquid flavorings effects on the lung innate immunity and the respiratory microbiota in lung injury.jpg
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| Description | Mechanisms of E-liquid flavorings effects on the lung innate immunity and the respiratory microbiota in lung injury. The respiratory tract is lined by a pseudostratified columnar ciliated epithelium (nasal cavity through the bronchi) transitioning to cuboidal on the bronchioles and squamous on the alveoli (AEC) (Khan and Lynch, 2020). The apical junctional complexes (AJC), including tight and adherens junctions (Yuksel and Turkeli, 2017), maintain the airways epithelial integrity and contribute to prevent contact between the respiratory microbiota and the phagocytic cells therefore, providing an immunotolerant environment an immunotolerant environment (Mathieu et al., 2018). At the AJC, the tight junctions regulate paracellular permeability and the adherens junctions provide cell-to-cell communication, while connecting to cellular cytoskeletal proteins (Hartsock and Nelson, 2008; Rezaee and Georas, 2014). The airway mucus (AM) constitutes the water-based apical layer of the airway surface liquid and the periciliary layer is the second sol-based layer that bathes the epithelium (Widdicombe, 2002a). The respiratory microbiota (RM) resembles the oral microbiota (OM). Members of the RM relies on the airway mucus to access nutrients including mucins (MUC5AC and MUC5B) and avoid contact with the epithelium, professional antigen presenter cells (DCs) and phagocytic cells such as alveolar macrophages (AMs) and neutrophils (PMNs). The airway epithelium secretes β-defensins and other host defense peptides and proteins (HDPs). In addition to the airway’s epithelium, the innate immune response within the respiratory tract involves phagocytic cells including dendritic cells, alveolar macrophages, neutrophils (Agostini et al., 1993; Allie and Randall, 2017); eosinophils (Mesnil et al., 2016); innate lymphoid cells and natural killer cells (Cong and Wei, 2019). The airway surface liquid represents an ecological niche for the respiratory microbiota, provides a source of specialized nutrients, and plays a role in immunomodulation by regulating the interaction between the respiratory microbiota and the immune system (Hoskins and Zamcheck, 1968; Ouwerkerk et al., 2013; Sommariva et al., 2020). ENDS flavorings such as cinnamaldehyde, menthol, or vanillin can disrupt microbial clearance in the respiratory tract by disrupting the AEC integrity and decreasing the levels of mucus, decreasing mucus clearance and antimicrobial secretion, and eliciting and inflammatory response, eventually producing lung injury. ENDS flavorings also impair the phagocytic activity of AMs and PMNs. Further research is needed to understand how changes induced by ENDS flavorings in the OM, alveolar macrophages phagocytic activity, NETosis, induced by ENDS flavors, may alter de RM eventually producing lung injury. |
| Date | |
| Source | https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2020.589501/full |
| Author | Zahira Quinones Tavarez, Dongmei Li, Daniel P. Croft, Steven R. Gill, Deborah J. Ossip, Irfan Rahman |
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| current | 10:29, 16 February 2024 | | 1,804 × 1,866 (277 KB) | Ameisenigel (talk | contribs) | {{Information |Description=Mechanisms of E-liquid flavorings effects on the lung innate immunity and the respiratory microbiota in lung injury. The respiratory tract is lined by a pseudostratified columnar ciliated epithelium (nasal cavity through the bronchi) transitioning to cuboidal on the bronchioles and squamous on the alveoli (AEC) (Khan and Lynch, 2020). The apical junctional complexes (AJC), including tight and adherens junctions (Yuksel and Turkeli, 2017), maintain the airways epithe... |
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