The cytoprotective effects of leukemia inhibitory factor during bacterial pneumonia

Pneumonia is a worldwide public health concern representing a leading burden of disease. During bacterial pneumonia, the alveolar-capillary barrier is critical for maintaining gas exchange and providing antimicrobial as well as pro-immune properties. Our group had previously demonstrated that leukemia inhibitory factor (LIF), an IL-6 family cytokine, is produced by type II alveolar epithelial cells (ATII) and is critical for tissue protection during bacterial pneumonia. However, cellular targets and signaling networks required for LIF-mediated protection are unknown. Here, we found that antibody-induced LIF blockade remodels the lung epithelial transcriptome in association with increased apoptosis. Based on these data, we performed pneumonia studies using a novel mouse model in which LIFR (the unique receptor for LIF) is absent in lung epithelium. LIFR is expressed on the surface of epithelial cells, and its absence elicited a significant increase in lung injury during pneumonia. Additionally, exogenous recombinant murine LIF administration into the lungs of wildtype mice had a modest but significant effect on pneumonia outcome. Finally, single-cell RNA sequencing (scRNAseq) was conducted to identify adult murine lung cell types most prominently expressing Lifr, revealing endothelial cells, mesenchymal cells, and ATIIs as major sources of Lifr. Sequencing data indicated that ATII cells were significantly impacted by pneumonia, with additional differences observed in response to LIF neutralization, including but not limited to gene programs related to cell death, injury, and inflammation. Overall, our data suggest that LIF signaling on epithelial cells alters responses in this cell type during pneumonia. However, given relatively modest albeit significant effects of epithelial LIFR deletion, our results also suggest separate and perhaps more prominent roles of LIFR in other cell types, such as endothelial cells or mesenchymal cells, which provide grounds for future investigation. To our knowledge, our findings are the first to identify cellular sources of Lifr mRNA with and without pneumonia and are also the first to demonstrate epithelial-specific consequences of LIF signaling in this context

Procedure Video (right click to open video in new tab)

Video depicting an example session

Reexamining the effect of gustatory disgust on moral judgment: A multi-lab direct replication of Eskine, Kacinik, and Prinz (2011)

This is the homepage for the meta-analysis of CREP replications for a "A Bad Taste in the Mouth: Gustatory Disgust Influences Moral Judgment" (Eskine, Kacinik, Prinz, 2011)

Contrasting academic and lay press print coverage of the 2013-2016 Ebola Virus Disease outbreak

<div><p>Under a traditional paradigm, only those with the expected background knowledge consume academic literature. The lay press, as well as government and non-government agencies, play a complementary role of extracting findings of high interest or importance and translating them for general viewing. The need for accurate reporting and public advising is paramount when attempting to tackle epidemic outbreaks through behavior change. Yet, public trust in media outlets is at a historic low. The Crisis and Emergency Risk Communication (CERC) model for media reporting on public health emergencies was established in 2005 and has subsequently been used to analyze media reporting on outbreaks of influenza and measles as well as smoking habits and medication compliance. However, no media analysis had yet been performed on the 2013–2016 Ebola Virus Disease (EVD) outbreak. This study compared the EVD information relayed by lay press sources with general review articles in the academic literature through a mixed-methods analysis. These findings suggest that comprehensive review articles could not serve as a source to clarify and contextualize the uncertainties around the EVD outbreak, perhaps due to adherence to technical accuracy at the expense of clarity within the context of outbreak conditions. This finding does not imply inferiority of the academic literature, nor does it draw direct causation between confusion in review articles and public misunderstanding. Given the erosion of the barriers siloing academia, combined with the demands of today’s fast-paced media environment, contemporary researchers should realize that no study is outside the public forum and to therefore consider shifting the paradigm to take personal responsibility in the process of accurately translating their scientific words into public policy actions to best serve as a source of clarity.</p></div