Human monocytes are divided into 3 major populations: classical (CD14+CD16-), non-classical (CD14dimCD16+), and intermediate (CD14+CD16+), each playing distinct roles in inflammation and immune responses. Trained immunity describes the long-term epigenetic and metabolic programming in innate immune cells in response to past insults, allowing enhanced responses against secondary infection. This is due to histone modifications causing long-term opening of chromatin at specific gene promoters after the immune activation status returns to baseline, as well as upregulation of both aerobic glycolysis and oxidative phosphorylation.
This research project investigates the effects of cigarette and e-cigarette usage on the proportion of human monocyte subsets and their production of pro-inflammatory cytokines in response to LPS and Streptococcus pneumoniae, potentially revealing a priming effect due to smoke exposure. The overall aim is to find whether cigarette smoke (CS) and vape smoke (VS) can induce memory-like responses in human monocytes. Although this allows for a broad-spectrum enhancement of the immune response, chronic “training” through exposure to continuous stimuli such as smoke has implications for aberrant inflammation characteristic of diseases such as COPD.
I hypothesize that both traditional and electronic smoke alters the immunological memory of monocytes, causing greater populations of non-classical monocytes and greater release of pro-inflammatory cytokines upon subsequent exposure to pathogenic insults, compared to monocytes of those who do not smoke. This effect may even be greater in dual users, who are exposed to a higher diversity of toxicants and reactive compounds.