Dr Johnson is a Lecturer and Principal Investigator at Aston University in Birmingham, UK. Dr Johnson’s current research interests focus on the role of pericytes in chronic lung disease, specifically investigating the progenitor cell capacity of these cells and their ability to contribute to the pathogenesis of pulmonary fibrosis.
Dr Johnson received her PhD in 2007 from McMaster University in Hamilton, Ontario, Canada with a focus on the biology of allergic asthma. She subsequently moved to the Karolinska Institute in Stockholm, Sweden as a postdoctoral fellow in the laboratory of Dr Jonas Fuxe to perform studies on the transcriptional regulation of epithelial-mesenchymal transition in cancer and allergic asthma. Dr Johnson then took up a second postdoctoral fellowship carried out in the laboratory of Prof Qutayba Hamid at the Meakins-Christie Laboratories at McGill University in Montréal, Québec, Canada to investigate epithelial-mesenchymal transition in primary bronchial epithelial cells derived from healthy subjects and severe asthmatics. Dr Johnson then held a Research Fellow position at Imperial College London from December 2011 to April 2016 in the Leukocyte Biology section of the National Heart and Lung Institute, Faculty of Medicine where she began studying the role of tissue-resident mesenchymal progenitor cells (pericytes) in driving lung fibrosis.
Other activities include working as a freelance proofreader, teaching immunology at the undergraduate and graduate levels, and performing peer reviews for a number of journals in the respiratory field and in general biological sciences. Jill has organized and taken part in an number of public engagement events such as Science Uncovered at the Natural History Museum, MRC Centenary events at the Science Museum and Southbank Observation Point, and Synapse with Girlguiding, and is a member of ScienceGrrl, a grassroots organisation celebrating and supporting women in science.
Areas of Expertise (5)
Chronic Lung Disease
McMaster University: PhD, Health Sciences 2007
McMaster University: BSc in Honours, Biology and Pharmacology 2002
- Member of the British Society for Immunology
Media Appearances (4)
Asthma: Scientists investigate new long-term treatment for relief beyond inhalers
Medical News Today online
“My personal opinion is that this novel drug would be ideally delivered in a combined formulation puffer with a long-acting bronchodilator, a corticosteroid to suppress inflammation. [I]n this way, both the inflammatory and structural aspects of allergic asthma could be more effectively treated and lead to an improved quality of life for the patient.” — Dr. Jill Johnson
Scientists Make Potential Breakthrough In Long-Term Asthma Treatment (In Mice)
“By targeting the changes in the airway directly, we hope this approach could eventually offer a more permanent and effective treatment than those already available, particularly for severe asthmatics who don’t respond to steroids,” Dr Jill Johnson, a Senior Lecturer at the University of Aston School of Biosciences and lead author of the study, said in a statement.
Potential long-term treatment for asthma found
Medical Xpress online
Lead researcher, Dr. Jill Johnson, from Aston University's School of Biosciences, says that "by targeting the changes in the airway directly, we hope this approach could eventually offer a more permanent and effective treatment than those already available, particularly for severe asthmatics who don't respond to steroids. However, our work is still at an early stage and further research is needed before we can begin to test this in people."
Potential long-term treatment for asthma found
Lead researcher, Dr Jill Johnson, from Aston University’s School of Biosciences, said: “By targeting the changes in the airway directly, we hope this approach could eventually offer a more permanent and effective treatment than those already available, particularly for severe asthmatics who don’t respond to steroids. However, our work is still at an early stage and further research is needed before we can begin to test this in people.”
Chemokine CXCL12 drives pericyte accumulation and airway remodeling in allergic airway diseaseRespiratory Research
2022 Background Airway remodeling is a significant contributor to impaired lung function in chronic allergic airway disease. Currently, no therapy exists that is capable of targeting these structural changes and the consequent loss of function. In the context of chronic allergic inflammation, pericytes have been shown to uncouple from the pulmonary microvasculature, migrate to areas of inflammation, and significantly contribute to airway wall remodeling and lung dysfunction. This study aimed to elucidate the mechanism by which pulmonary pericytes accumulate in the airway wall in a model of chronic allergic airway inflammation. Methods Mice were subjected to a protocol of chronic airway inflammation driven by the common environmental aeroallergen house dust mite. Phenotypic changes to lung pericytes were assessed by flow cytometry and immunostaining, and the functional capacity of these cells was evaluated using in vitro migration assays. The molecular mechanisms driving these processes were targeted pharmacologically in vivo and in vitro. Results Pericytes demonstrated increased CXCR4 expression in response to chronic allergic inflammation and migrated more readily to its cognate chemokine, CXCL12. This increase in migratory capacity was accompanied by pericyte accumulation in the airway wall, increased smooth muscle thickness, and symptoms of respiratory distress. Pericyte uncoupling from pulmonary vessels and subsequent migration to the airway wall were abrogated following topical treatment with the CXCL12 neutraligand LIT-927. Conclusion These results provide new insight into the role of the CXCL12/CXCR4 signaling axis in promoting pulmonary pericyte accumulation and airway remodeling and validate a novel target to address tissue remodeling associated with chronic inflammation.
Baseline Characteristics and Outcomes After Anti–Vascular Endothelial Growth Factor Therapy for Macular Edema in Participants With Hemiretinal Vein Occlusion Compared With Participants With [...]JAMA Ophthalmology
2022 Importance Intravitreal anti–vascular endothelial growth factor (VEGF) injections are commonly used to treat eyes with macular edema secondary to hemiretinal vein occlusion (HRVO) or central retinal vein occlusion (CRVO). Information on whether differences exist in outcomes after anti-VEGF therapy can help guide treatment for each of the different disease types. Objective To compare baseline characteristics, treatment burden, and outcomes of macular edema treatment in participants with HRVO with those of participants with CRVO. Design, Setting, and Participants This post hoc outcome analysis from the Study of Comparative Treatments for Retinal Vein Occlusion 2 randomized clinical trial included 362 participants with macular edema caused by HRVO or CRVO treated at 66 US sites. Randomization began in September 2014, and the last month 24 follow-up visit occurred in February 2018. Data were analyzed from April 2020 to May 2021. Interventions Eyes were initially randomized to 6 monthly intravitreal injections of aflibercept or bevacizumab and were treated according to protocol between months 6 to 12 depending on 6-month outcome. After month 12, patients were treated per investigator discretion and observed through month 60.
Support of human alveolar organoid growth by pulmonary endothelial cells: possible influence of cigarette smoke exposureERJ Open Research
2022 mphysema is a component of Chronic Obstructive Pulmonary Disease (COPD) and is characterized by destruction of alveolar walls, which includes alveolar epithelial, endothelial and mesenchymal cells. It is increasingly realized that microvascular endothelial cell (dys)function contributes to emphysema development. The aim is to study the mechanistic interactions of human pulmonary microvascular endothelial and alveolar cells CD31+ pulmonary endothelial cells were isolated from human resected lung tissue homogenate, and expanded in vitro. Endothelial cells at passage 2 (P2)(n=3) were allowed to form a monolayer in the bottom of a culture plate (no fibroblasts added), that contained an insert with freshly isolated HTII-280+ alveolar cells from human resected lung tissue, were seeded in basement membrane extract matrix Co-culture of alveolar type 2 cells with primary lung endothelial cells increased (2.3-fold) human alveolar organoid number after 10 days. This finding supports a role for pulmonary endothelial cells in alveolar cell progenitor functioning. Next, endothelial cells (n=4) at P2, were exposed to 1, 2.5 or 5 arbitrary units (AU)/ml of cigarette smoke extract (CSE) for 1, 4 and 24 hours. Exposure of pulmonary endothelial cells to CSE reduced expression of genes involved in alveolar support (TMEM100, ALK1, BMPR1, MMP14, TSP-1) at 24hrs in a concentration-dependent manner. Expression of stress response genes (HMOX1, NQO1, GADD34 and spliced XBP1) increased at 24 hours in all concentrations of CSE. We are currently analyzing the impact of COPD-associated triggers such as cigarette smoke on endothelial cell-driven alveolar organoid formation.