A predicted rapid growth in science, technology, engineering, and math (STEM) careers demands a vast and talented workforce, but students most commonly abandon STEM majors within the first 2 years of college. Performance in introductory courses, scientific literacy, and the ability to critically reason are main predictors of retention in STEM, highlighting the importance of precollege and early college experience. The Life Science Research Immersion Program (LSRIP) is a novel science education model that focuses on the development of scientific research skills, thus preparing students for introductory college courses and beyond. To evaluate the efficacy of the LSRIP, pre- and postprogram assessments and surveys were administered to three precollege student cohorts. Scientific reasoning assessment scores improved by 4.70% in Summer 2019 (P < 0.01), 9.44% in Fall 2019 (P < 0.05), and 0.97% in Winter 2020 cohorts, with two of five questions showing statistically significant improvement. Surveyed attitudes toward science improved in 62.9% of questions across all cohorts. These results suggest that research immersion experiences are an effective educational instrument for improving and promoting scientific reasoning and attitudes among precollege students. To better prepare students for success in STEM higher education and careers, we recommend implementing LSRIPs to complement traditional precollege science curricula.

Background

Individuals with certain chronic inflammatory lung diseases have a higher risk of developing lung cancer (LC). However, the underlying mechanisms remain largely unknown. Here, we hypothesized that chronic exposure to house dust mites (HDM), a common indoor aeroallergen associated with the development of asthma, accelerates LC development through the induction of chronic lung inflammation (CLI).  METHODS: The effects of HDM and heat-inactivated HDM (HI-HDM) extracts were evaluated in two preclinical mouse models of LC (a chemically-induced model using the carcinogen urethane and a genetically-driven model with oncogenic Kras^G12D activation in lung epithelial cells) and on murine macrophages in vitro. Pharmacological blockade or genetic deletion of the Nod-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasome, caspase-1, interleukin-1β (IL-1β), and C-C motif chemokine ligand 2 (CCL2) or treatment with an inhaled corticosteroid (ICS) was used to uncover the pro-tumorigenic effect of HDM.  RESULTS: Chronic intranasal (i.n) instillation of HDM accelerated LC development in the two mouse models. Mechanistically, HDM caused a particular subtype of CLI, in which the NLRP3/IL-1β signaling pathway is chronically activated in macrophages, and made the lung microenvironment conducive to tumor development. The tumor-promoting effect of HDM was significantly decreased by heat treatment of the HDM extract and was inhibited by NLRP3, IL-1β, and CCL2 neutralization, or ICS treatment.

Conclusions

Collectively, these data indicate that long-term exposure to HDM can accelerate lung tumorigenesis in susceptible hosts (e.g., mice and potentially humans exposed to lung carcinogens or genetically predisposed to develop LC).