Monday, November 18, 2019

Electronic Cigarettes Disrupt Lung Lipid Homeostasis and Innate Immunity Independent of Nicotine


The US has seen a vaping crisis lately.  The problem began showing up around med-summer and continues to today.  The documented cases show that greater than 200 patients have been affected so far.

One of the frightening things about this problem is that it is showing up in young people who are normally expected to be in the prime of physical health.  The numbers are probably trending to youth simply because the vaping fad is heaviest in that demographic.  Current stats are showing that around 20 percent of high school students are vaping.

The disease/problem presents as a “pneumonia-type” situation.  Patients who are otherwise healthy are suddenly having trouble breathing.  Some are having chest pain, vomiting, and diarrhea.  The patients present with these problems and yet they test negative for bacterial and virus infections.  The only thing these cases seem to have in common is that every patient reported having recently used an e-cigarette.

Now a study published in The Journal of Clinical Investigation is showing that the body’s way of protecting the lungs is damaged by the contents of vape pods; even those that do not contain nicotine.

Here is the abstract:

Electronic nicotine delivery systems (ENDS) or e-cigarettes have emerged as a popular recreational tool among adolescents and adults. Although the use of ENDS is often promoted as a safer alternative to conventional cigarettes, few comprehensive studies have assessed the long-term effects of vaporized nicotine and its associated solvents, propylene glycol (PG) and vegetable glycerin (VG). Here, we show that compared with smoke exposure, mice receiving ENDS vapor for 4 months failed to develop pulmonary inflammation or emphysema. However, ENDS exposure, independent of nicotine, altered lung lipid homeostasis in alveolar macrophages and epithelial cells. Comprehensive lipidomic and structural analyses of the lungs revealed aberrant phospholipids in alveolar macrophages and increased surfactant-associated phospholipids in the airway. In addition to ENDS-induced lipid deposition, chronic ENDS vapor exposure downregulated innate immunity against viral pathogens in resident macrophages. Moreover, independent of nicotine, ENDS-exposed mice infected with influenza demonstrated enhanced lung inflammation and tissue damage. Together, our findings reveal that chronic e-cigarette vapor aberrantly alters the physiology of lung epithelial cells and resident immune cells and promotes poor response to infectious challenge. Notably, alterations in lipid homeostasis and immune impairment are independent of nicotine, thereby warranting more extensive investigations of the vehicle solvents used in e-cigarettes.

The study is a pretty fascinating read for those of you with a science or healthcare background.  The entire study can be accessed with this link.  

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