Purpose : This repository is a data analysis practice project using publicly available bulk RNA sequencing data (GSE183973). My intention is to compare and contrast various R packages such as DESeq2, EdgeR, limma & voom. A completed project will consist of PCA plots, volcano plots, heatmaps, over-representation analysis and gene enrichment analysis. Once completed i intend to practice data presentation for the general public in a format such as Power Bi.
Title : Airway Macrophages Encompass Transcriptionally and Functionally Distinct Subsets Altered by Smoking
Authors : Maude Liegeois, Qiang Bai, Laurence Fievez, Dimitri Pirottin, Celine Legrand, Julien Guiot, Florence Schleich, Jean-Louis Corhay, Renaud Louis, Thomas Maricha, and Fabrice Bureau
Abstract : Alveolar macrophages (AMs) are functionally important innate cells involved in lung homeostasis and immunity and whose diversity in health and disease is a subject of intense investigations. Yet, it remains unclear to what extent conditions like smoking or chronic obstructive pulmonary disease (COPD) trigger changes in the AM compartment. Here, we aimed to explore heterogeneity of human AMs isolated from healthy nonsmokers, smokers without COPD, and smokers with COPD by analyzing BAL fluid cells by flow cytometry and bulk and single-cell RNA sequencing. We found that subpopulations of BAL fluid CD2061 macrophages could be distinguished based on their degree of autofluorescence in each subject analyzed. CD2061 autofluorescenthigh AMs were identified as classical, self-proliferative AM, whereas autofluorescentlow AMs were expressing both monocyte and classical AM-related genes, supportive of a monocytic origin. Of note, monocyte-derived autofluorescentlow AMs exhibited a functionally distinct immunoregulatory profile, including the ability to secrete the immunosuppressive cytokine IL-10. Interestingly, single-cell RNA-sequencing analyses showed that transcriptionally distinct clusters of classical and monocyte-derived AM were uniquely enriched in smokers with and without COPD as compared with healthy nonsmokers. Of note, such smoking-associated clusters exhibited gene signatures enriched in detoxification, oxidative stress, and proinflammatory responses. Our study independently confirms previous reports supporting that monocyte-derived macrophages coexist with classical AM in the airways of healthy subjects and patients with COPD and identifies smoking-associated changes in the AM compartment that may favor COPD initiation or progression.