ORCID Profile
0000-0002-5091-2660
Current Organisation
University of California, San Diego
Does something not look right? The information on this page has been harvested from data sources that may not be up to date. We continue to work with information providers to improve coverage and quality. To report an issue, use the Feedback Form.
Publisher: American Physiological Society
Date: 04-2021
DOI: 10.1152/AJPLUNG.00370.2020
Abstract: The growing interest in regulating flavored E-liquids must incorporate understanding of the “flavoring profile” of each E-liquid—which flavorings (flavoring chemicals) are present and at what concentrations not just focusing on the flavor on the label. We investigated the flavoring profile of 10 different flavored E-liquids. We assessed bronchial epithelial cell viability and apoptosis, phagocytosis of bacteria and apoptotic cells by macrophages after exposure to E-cigarette vapor extract (EVE). We validated our data in normal human bronchial epithelial cells (NHBE) and alveolar macrophages (AM) from healthy donors. We also assessed cytokine release and validated in the saliva from E-cigarette users. Increased necrosis/apoptosis (16.1–64.5% apoptosis) in 16HBE cells was flavor dependent, and NHBEs showed an increased susceptibility to flavors. In THP-1 differentiated macrophages phagocytosis was also flavor dependent, with AM also showing increased susceptibility to flavors. Further, Banana and Chocolate were shown to reduce surface expression of phagocytic target recognition receptors on alveolar macrophages. Banana and Chocolate increased IL-8 secretion by NHBE, whereas all 4 flavors reduced AM IL-1β secretion, which was also reduced in the saliva of E-cigarette users compared with healthy controls. Flavorant profiles of E-liquids varied from simple 2 compound mixtures to complex mixtures containing over a dozen flavorants. E-liquids with high benzene content, complex flavoring profiles, high chemical concentration had the greatest impacts. The Flavorant profile of E-liquids is key to disruption of the airway status quo by increasing bronchial epithelial cell apoptosis, causing alveolar macrophage phagocytic dysfunction, and altering airway cytokines.
Publisher: Springer Science and Business Media LLC
Date: 30-03-2022
Publisher: American Association for the Advancement of Science (AAAS)
Date: 20-08-2021
Abstract: Changes in lung ACE2 expression and apoptotic priming throughout life span may affect COVID severity.
Publisher: Cold Spring Harbor Laboratory
Date: 31-10-2019
DOI: 10.1101/825836
Abstract: How obesity affects immune function is not well understood. Clinically, obesity is strongly associated with severe T H 2 immunopathology 1-3 , though the physiological, cellular, and molecular underpinnings of this association remain obscure. Here, we demonstrate that obese mice are susceptible to severe atopic dermatitis (AD), a major manifestation of T H 2 immunopathology and disease burden in humans 4,5 . Mechanistically, we show that dysregulation of the nuclear hormone receptor (NHR) PPAR γ (peroxisome proliferator-activated receptor gamma) in T cells is a causal link between obesity and the increased T H 2 immunopathology. We find that PPAR γ oversees a cellular metabolic transcriptional program that restrains nuclear gene expression of the chief T H 2 priming and effector cytokine interleukin-4 (IL-4). Accordingly, thiazolidinediones (TZDs), potent PPAR γ agonists, robustly protect obese mice from T H 2 immunopathology. Collectively, these findings establish PPAR γ as a molecular link between obesity and T H 2 immune homeostasis and identify TZDs as novel therapeutic candidates for T H 2 immunopathology. Fundamentally, these findings demonstrate that shifting physiologic metabolic states can shape the tone of adaptive immune responses to modulate differential disease susceptibility.
Location: United States of America
Location: United States of America
No related grants have been discovered for Laura Crotty Alexander.