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Using murine smoke models and single-cell RNA-sequencing, we show that smoking establishes a self-amplifying inflammatory loop characterized by an influx of molecularly heterogeneous neutrophil subsets and excessive recruitment of monocyte-derived alveolar macrophages (MoAM)

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As enjoyment of nicotines pleasurable effects are hypothesized mechanisms in the catalyst model, studies of whether e-cigarette nicotine concentration is associated with smoking were also considered as relevant to determining plausibility