A5023482526- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Immune Response and Inflammation
- Immune cells in cancer
- Neonatal Respiratory Health Research
- Immune Cell Function and Interaction
- Inhalation and Respiratory Drug Delivery
- Pulmonary Hypertension Research and Treatments
- Hematopoietic Stem Cell Transplantation
- Chronic Obstructive Pulmonary Disease (COPD) Research
- Immunotherapy and Immune Responses
- Wound Healing and Treatments
- Cytomegalovirus and herpesvirus research
- Occupational exposure and asthma
- T-cell and B-cell Immunology
- Asthma and respiratory diseases
- Pleural and Pulmonary Diseases
- Respiratory Support and Mechanisms
- Respiratory viral infections research
- Medical Imaging and Pathology Studies
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- IL-33, ST2, and ILC Pathways
- Occupational and environmental lung diseases
- Transplantation: Methods and Outcomes
- Inflammatory mediators and NSAID effects
- Gut microbiota and health
University of Michigan
2016-2025
Michigan Medicine
2005-2024
Michigan United
2006-2024
University of Wisconsin–Madison
2024
Madison Group (United States)
2024
Ann Arbor Center for Independent Living
2010-2023
University of Bristol
2008-2023
Bethany College - West Virginia
2010-2023
Sandia National Laboratories California
2022
Pulmonary and Critical Care Associates
2010-2021
Section:ChooseTop of pageAbstract <<CONTENTSI. STATEMENT OF THE PROBL...II. WHAT IS BEING MODELED...III. METHODOLOGYIV. RESULTS: FEATURES AND...V. PRACTICAL ASPECTS M...VI. CRITICAL ASSESSMENT O...VII. LIMITATIONSVIII. SUMMARY AND CONCLUS...ReferencesCITING ARTICLES
Rationale: Extracellular matrix (ECM) is a dynamic tissue that contributes to organ integrity and function, its regulation of cell phenotype major aspect biology. However, standard in vitro culture approaches are unclear physiologic relevance because they do not mimic the compositional, architectural, or distensible nature living organ. In lung, fibroblasts exist ECM-rich interstitial spaces key effectors lung fibrogenesis.Objectives: To better address how ECM influences fibroblast...
Ineffective repair of a damaged alveolar epithelium has been postulated to cause pulmonary fibrosis. In support this theory, epithelial cell abnormalities, including hyperplasia, apoptosis, and persistent denudation the basement membrane, are found in lungs humans with idiopathic fibrosis animal models fibrotic lung disease. Furthermore, mutations genes that affect regenerative capacity or injury/apoptosis type II cells have identified familial forms Although these findings compelling, there...
The present study was designed to elucidate the effects of chemokine monocyte chemoattractant protein (MCP-1) on blood–brain barrier (BBB) permeability. Experiments were conducted under in vitro conditions (coculture brain endothelial cells and astrocytes) cellular MCP-1 vivo (intracerebral intracerebroventricular administration MCP-1) potential contribution BBB disruption vivo. Our results showed that induces a significant increase permeability surface area product for fluorescein...
Numerous compounds have shown efficacy in limiting development of pulmonary fibrosis using animal models, yet few these replicated beneficial effects clinical trials. Given the challenges associated with performing trials patients idiopathic (IPF), it is imperative that preclinical data packages be robust their analyses and interpretations to best chance selecting promising drug candidates advance The American Thoracic Society has convened a group experts lung discuss formalize...
Idiopathic pulmonary fibrosis (IPF) causes considerable global morbidity and mortality, its mechanisms of disease progression are poorly understood. Recent observational studies have reported associations between lung dysbiosis, altered host defense gene expression, supporting a role for microbiota in IPF. However, the causal significance is undetermined.
Idiopathic pulmonary fibrosis (IPF) is a progressive fibrotic lung disease without effective therapeutics. Periostin has been reported to be elevated in IPF patients relative controls, but its sources and mechanisms of action remain unclear. We confirm excess periostin lungs show that fibroblasts produce periostin. Blood was obtained from 54 (all 1 with 48 wk follow-up). levels predict clinical progression at (hazard ratio = 1.47, 95% confidence interval 1.03–2.10, P < 0.05). Monocytes...
Section:ChooseTop of pageAbstract <<Biology Alveolar Injur...Role ECMPreclinical ModelingThe Role Inflammation ...Genetic, Epigenetic, and ...Translation Discoverie...SummaryReferencesCITING ARTICLES
There is an urgent need for biomarkers to better stratify patients with idiopathic pulmonary fibrosis by risk lung transplantation allocation who have the same clinical presentation. We aimed investigate whether a specific immune cell type from could identify those at higher of poor outcomes. then sought validate our findings using cytometry and electronic health records.
Wound monocyte-derived macrophage plasticity controls the initiation and resolution of inflammation that is critical for proper healing, however, in diabetes mellitus, fails to occur. In diabetic wounds, kinetics blood monocyte recruitment mechanisms control vivo monocyte/macrophage differentiation remain unknown.Here, we characterized function Ly6CHi [Lin- (CD3-CD19-NK1.1-Ter-119-) Ly6G-CD11b+] Ly6CLo subsets normal wounds. Using flow-sorted tdTomato-labeled monocyte/macrophages, show cells...
Advancements in methods, technology, and our understanding of the pathobiology lung injury have created need to update definition experimental acute (ALI). We queried 50 participants with expertise ALI respiratory distress syndrome using a Delphi method composed series electronic surveys virtual workshop. propose that presents as “multidimensional entity” characterized by four “domains” reflect key pathophysiologic features underlying biology human syndrome. These domains are 1) histological...
Macrophage plasticity is critical for normal tissue repair following injury. In pathologic states such as diabetes, macrophage impaired, and macrophages remain in a persistent proinflammatory state; however, the reasons this are unknown. Here, using single-cell RNA sequencing of human diabetic wounds, we identified increased JMJD3 wound macrophages, resulting inflammatory gene expression. Mechanistically, report that healing, directs early macrophage-mediated inflammation via JAK1,3/STAT3...
Idiopathic Pulmonary Fibrosis (IPF) is a progressive scarring disease arising from impaired regeneration of the alveolar epithelium after injury. During regeneration, type 2 epithelial cells (AEC2s) assume transitional state that upregulates multiple keratins, and ultimately differentiate into AEC1s. In IPF, AECs accumulate with ineffectual AEC1 differentiation. However, whether how cause fibrosis, keratins regulate cell accumulation why fibrosis resolve in mouse models but IPF are unclear....
Idiopathic pulmonary fibrosis (IPF) is characterized by progressive scarring and loss of lung function. With limited treatment options, patients succumb to the disease within 2 5 years. The molecular pathogenesis IPF regarding immunologic changes that occur poorly understood. We characterize a role for non-canonical aryl-hydrocarbon receptor signaling (ncAHR) in dendritic cells (DCs) leads production IL-6 increased IL-17+ cells, promoting fibrosis. TLR9 myofibroblasts shown regulate TDO2...
Abstract Pulmonary fibrosis can be modeled in animals by intratracheal instillation of FITC, which results acute lung injury, inflammation, and extracellular matrix deposition. We have previously shown that despite chronic this model pulmonary is lymphocyte independent. The CC chemokine monocyte-chemoattractant protein-1 induced following FITC Therefore, we investigated the contribution main receptor, CCR2, to fibrotic disease process. demonstrate CCR2−/− mice are protected from both...
We have previously shown that mice are genetically deficient in the CCR2 gene (CCR2-/- mice) protected from fluorescein isothiocyanate (FITC)-induced lung fibrosis. Protection fibrosis correlated with impaired recruitment of fibrocytes (bone marrow-derived cells, which share both leukocyte and mesenchymal markers). There three ligands for mouse: CCL2, CCL7, CCL12. CCL2 CCL12 elevated after FITC injury, but different kinetics. is maximal at Day 1 absent by 7 FITC. In contrast, peaks 3,...