miR-223:A Key Regulator in the Innate Immune Response in Asthma and COPD

Asthma and Chronic Obstructive Pulmonary Disease (COPD) are chronic obstructive respiratory diseases characterized by airway obstruction, inflammation, and remodeling. Recent findings indicate the importance of microRNAs (miRNAs) in the regulation ofpathological processes involved in both diseases. MiRNAs have been implicated in a wide array of biological processes, such as inflammation, cell proliferation, differentiation, and death. MiR-223 is one of the miRNAs that is thought to play a role in obstructive lung disease as altered expression levels have been observed in both asthma and COPD. MiR-223 is a hematopoietic cell–derived miRNA that plays a role in regulation of monocyte-macrophage differentiation, neutrophil recruitment, and pro-inflammatory responses and that can be transferred to non-myeloid cells via extracellular vesicles or lipoproteins. In this translational review, we highlight the role of miR-223 in obstructive respiratory diseases, focusing on expression data in clinical samples of asthma and COPD, in vivo experiments in mouse models and in vitro functional studies. Furthermore, we provide an overview of the mechanisms by which miR-223 regulates gene expression. We specifically focus on immune cell development and activation and involvement in immune responses, which are important in asthma and COPD. Collectively, this review demonstrates the importance of miR-223 in obstructive respiratory diseases and explores its therapeutic potential in the pathogenesis of asthma and COPD. <br/

miR-223 : a key regulator in the innate immune response in asthma and COPD

Asthma and Chronic Obstructive Pulmonary Disease (COPD) are chronic obstructive respiratory diseases characterized by airway obstruction, inflammation, and remodeling. Recent findings indicate the importance of microRNAs (miRNAs) in the regulation of pathological processes involved in both diseases. MiRNAs have been implicated in a wide array of biological processes, such as inflammation, cell proliferation, differentiation, and death. MiR-223 is one of the miRNAs that is thought to play a role in obstructive lung disease as altered expression levels have been observed in both asthma and COPD. MiR-223 is a hematopoietic cell-derived miRNA that plays a role in regulation of monocyte-macrophage differentiation, neutrophil recruitment, and pro-inflammatory responses and that can be transferred to non-myeloid cells via extracellular vesicles or lipoproteins. In this translational review, we highlight the role of miR-223 in obstructive respiratory diseases, focusing on expression data in clinical samples of asthma and COPD, in vivo experiments in mouse models and in vitro functional studies. Furthermore, we provide an overview of the mechanisms by which miR-223 regulates gene expression. We specifically focus on immune cell development and activation and involvement in immune responses, which are important in asthma and COPD. Collectively, this review demonstrates the importance of miR-223 in obstructive respiratory diseases and explores its therapeutic potential in the pathogenesis of asthma and COPD

Let’s Keep in Touch:Strong Cell-cell Contacts for Healthy Lungs

Prof Irene Heijink (1975) and her team study the mechanisms underlying lung tissue damage in various lung diseases, such as asthma, COPD and pulmonary fibrosis She does this in close collaboration with the clinic, using culture models with cells derived from patients. Heijink directs the Experimental Lung Diseases Lab (EXPIRE) and is currently programme leader of the Groningen Research Institute for COPD (GRIAC), a multidisciplinary and translational research institute in which close collaboration takes place between basic and clinical scientists.Lung diseases are a major social problem. Diseases such as asthma and COPD are common and have a major impact on quality of life. In fact, COPD is currently the third box cause worldwide. Lung diseases are often only detected at a late stage when there is already significant damage that is no longer treatable. In particular, damage to the lining layer of the airways and lungs (the epithelium - involved in immune processes) with loss of mutual contact between cells in this layer is currently seen as a crucial part of disease processes. Irene Heijink discovered that an important directing role is played by the damaged epithelium in the derailed inflammatory response in the lungs of asthma and COPD patients. In her Chair in Cellular and Molecular Lung Pathology, Heijink aims to develop new strategies to repair the epithelial barrier in lung diseases and thereby stop or even reverse the disease process. In doing so, she uses advanced culture models (such as lab-on-chip), which she is developing within a large national collaboration to detect lung damage earlier and find new leads for treatment. She is also developing a new strategy in collaboration with the University of Twente, using an innovative technology, to better treat damage deep in the lungs and possibly even achieve tissue repair