Open AccessAcute vaping exacerbates microbial pneumonia due to calcium (Ca2+) dysregulation
Author(s) -
Rui Zhang,
Myles M. Jones,
De’Jana Parker,
R E Dornsife,
Nathan Wymer,
Rob U. Onyenwoke,
Vijay Sivaraman
Publication year - 2021
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0256166
Subject(s) - lung , flow cytometry , inflammation , immunology , medicine , macrophage , pneumonia , pulmonary pathology , pathology , biology , cancer research , in vitro , biochemistry
As electronic cigarette (E-cig) use, also known as “vaping”, has rapidly increased in popularity, data regarding potential pathologic effects are recently emerging. Recent associations between vaping and lung pathology have led to an increased need to scrutinize E-cigs for adverse health impacts. Our previous work (and others) has associated vaping with Ca 2+ -dependent cytotoxicity in cultured human airway epithelial cells. Herein, we develop a vaped e-liquid pulmonary exposure mouse model to evaluate vaping effects in vivo . Using this model, we demonstrate lung pathology through the use of preclinical measures, that is, the lung wet: dry ratio and lung histology/H&E staining. Further, we demonstrate that acute vaping increases macrophage chemotaxis, which was ascertained using flow cytometry-based techniques, and inflammatory cytokine production, via Luminex analysis, through a Ca 2+ -dependent mechanism. This increase in macrophage activation appears to exacerbate pulmonary pathology resulting from microbial infection. Importantly, modulating Ca 2+ signaling may present a therapeutic direction for treatment against vaping-associated pulmonary inflammation.