Dr Farrah Kheradmand explains the mechanisms of lung injury due to vaporization

After 1 month, we started to see differences in the appearance of macrophages in mice exposed to e-cigarettes, nicotine-independent, said Farrah Kheradmand, MD, professor of pulmonary medicine at Baylor College of Medicine and member physician. of the Houston Veterans. Business Medical Center (VA). Kheradmand’s research was presented at this year’s American Thoracic Society (ATS) Virtual Conference 2021.


Can you provide an overview of your presentation “Mechanisms of Injury Caused by Vaping?”

We were very interested in the potential dangers of vaping with nicotine as an alternative to cigarettes. We did a very simple 2 by 2 experiment, as most of my VA patients wanted to know if vaping is safe, a safe alternative. This is how it was announced.

We took mice and exposed them to vaping with or without nicotine, and to cigarettes or air. We wanted to compare what happens to inflammatory mediators in cigarette smoke versus taking nicotine in the form of aerosol vaping. What we found is that they are completely different, which means that the inflammatory mediators that arrive in the lungs of mice when exposed to conventional cigarettes are completely different from those when you expose mice. to electronic cigarettes.

Interestingly, when we exposed them for a chronic period, which meant we didn’t want to know what the immediate response was, we wanted to know what was happening in the long term, because most people don’t just vape for 1 or 2 days. . They want to vape for a long time. Our experimental model was such that we could actually test this hypothesis. When we exposed mice to 4 months of cigarette smoke, we saw what we had seen before. Mice have emphysema, they receive inflammatory mediators, especially innate and adaptive immune cells in the lungs.

What we found was that while we didn’t see emphysema in mice exposed to e-cigarettes, the pulmonary macrophages – these are innate immune cells in the lungs – were markedly different from those mice exposed to air or cigarette smoke. What’s more interesting is that it doesn’t matter whether they’re exposed to nicotine or not. It happened regardless of the nicotine. This is really how the story began, as the altering alteration of innate immune cells in the lungs. It puts us on the path we have discovered.

Based on your research, what can happen to a person’s lungs when they vape?

What we found was that we exposed mice to e-cigarettes and as early as maybe a month after the start – and again we did a [exposure] which is almost like smoking a lifetime in a human lifetime, so 4 months of e-cigarettes – as early as 1 month we started to see differences in the appearance of macrophages, again, regardless of nicotine, in mice exposed to electronic cigarettes. When we identified the macrophages [they had] kind of shiny look. When we stained them for oil, and in these vacuoles, we found that there were large amounts of oil settling in the macrophages. That’s why they seemed more translucent, they seemed to have vacuoles in them.

We initially thought they were going through apoptosis, or cell death. But we looked at all the markers of it, and we didn’t identify any such activity. But what we researched and found was that there was an accumulation of lipids inside the cell body. When we opened the cells and took an unbiased approach to try to figure out what these lipids are, we found that they are actually lipids that are normally found in surfactants. Surfactant is that lubricant that keeps the alveoli open, so we can continue to keep our lungs open and breathe. What happens is that these particular molecules called surfactants are recycled – a third of the surfactant is recycled every hour.

It’s a very, very active process. Macrophages and type 2 alveolar cells are specialized cells inside the lung, they talk to each other, if you will. They actually coordinate the recycling of surfactants so that we always have a new layer of surfactant in our lungs to keep the lungs open. Part of the function of macrophages is to effectively perform this surfactant recycling. What we have assumed is that the function of the alveolar macrophages is disrupted, so that in order for them to recycle the surfactant, they cannot catch up. They therefore accumulate inside their cell body. That’s why over time it’s a cumulative thing.

While at about a month we see a few macrophages that have this glossy and fatty deposited, over time, at 3 or 4 months of exposure, we find almost the majority of cells that have this phenotype. This means that the more exposed you are, the more this process is delayed and the more the macrophages become dysfunctional.

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