Research Interests: Sarcoidosis Granulomatous Lung Diseases T cells Monocytes chemokines Summary: Dr. Koth's research program is structured around the study of samples from human research studies. With the breath of research techniques that can be applied to human samples to learn about disease, Dr. Koth is taking a direct approach in the study of lung diseases. Dr. Koth's current focus involves understanding the inflammatory disease called sarcoidosis. This is not a disease as common as asthma, but it affects both young and middle aged people and causes significant morbidity and mortality. More awareness and funds are needed if we hope to understand the complicated biology of the disease. For example, many of the main immune subsets of the body are abnormally regulated in this disease. Most research has focused on the traditional T-cell. For example, it is thought that specific T cells are very activated and making inflammatory products which are contributing to and continuing the disease. However there are other immune cells that have not been studied adequately. Dr. Koth's lab has taken an active interest in these other types of immune cells. One reason for this is that we have identified, using Genomics research, that specific transcripts in the blood actually predict whether a specific patient will have progressive disease or not. She and her lab are now pursuing a line of investigation to understand where this 'biomarker message' is coming from in order to be able to stop it. Dr. Koth's lab is also interested in using state-of-the-art technology to think about new therapies for this disease. We are looking into cutting-edge translational methods of expanding a type of immune cell responsible for down regulating the inflammatory process of the body. To perform these experiments in clinical trials will require significant financial support and we are seeking this input in order to move this very exciting potential treatment forward. The other aspect of my research program includes the development of a 'center of excellence in sarcoidosis'. This program will be designed to include both excellence in clinical care and novel clinical studies. Developing clinical care standards is an important area in managing sarcoidosis patients since sarcoidosis is a chronic disease that may be active for 10-20 years or more. Thus, a full-service clinical care program would facilitate the creation of clinical management tools and treatment regimens (developed as products from clinical trials networks) to address three arms of care in sarcoidosis: 1) organ damage, 2) symptom control, and 3) psychosocial aspects of living with the disease.
Publications
Plasma Proteomic Profiling Reveals Distinct Signatures of Chest CT Phenotypes in Sarcoidosis.
Discovery of Two Novel Immunoepitopes and Development of Peptide-based Sarcoidosis Immunoassay.
Response.
Examination of eQTL Polymorphisms Associated with Increased Risk of Progressive Complicated Sarcoidosis in European and African Descent Subjects.
Genome-wide association study identifies multiple HLA loci for sarcoidosis susceptibility.
Screening for Exposure to Beryllium Among US Veterans With a Diagnosis of Sarcoidosis, 2002-2020.
Epidemiology of Sarcoidosis in U.S. Veterans from 2003 to 2019.
Modulatory role of macrophage migration inhibitory factor on cytokines and clinical features of sarcoidosis.
Performance of a Computational Phenotyping Algorithm for Sarcoidosis Using Diagnostic Codes in Electronic Medical Records: Case Validation Study From 2 Veterans Affairs Medical Centers.
Transcriptomics of bronchoalveolar lavage cells identifies new molecular endotypes of sarcoidosis.
Neurosarcoidosis: Pathophysiology, Diagnosis, and Treatment.
Molecular profiling in sarcoidosis.
T-bet Expression in Peripheral Th17.0 Cells Is Associated With Pulmonary Function Changes in Sarcoidosis.
Diagnosis and Detection of Sarcoidosis. An Official American Thoracic Society Clinical Practice Guideline.
CXCL9 and CXCL10 are differentially associated with systemic organ involvement and pulmonary disease severity in sarcoidosis.
Long-Term Corticosteroid-Sparing Immunosuppression for Cardiac Sarcoidosis.
Serum CXCL11 correlates with pulmonary outcomes and disease burden in sarcoidosis.
Elastin-Specific Autoimmunity in Smokers With Thoracic Aortic Aneurysm and Dissection is Independent of Chronic Obstructive Pulmonary Disease.
Tissue Isn't the Issue.
Migraine is common in patients with sarcoidosis.
Sleep disturbance and symptom burden in sarcoidosis.
Increased T-helper 17.1 cells in sarcoidosis mediastinal lymph nodes.
Disease Burden and Variability in Sarcoidosis.
IFN-γ-Producing T-Helper 17.1 Cells Are Increased in Sarcoidosis and Are More Prevalent than T-Helper Type 1 Cells.
Rationale and Design of the Genomic Research in Alpha-1 Antitrypsin Deficiency and Sarcoidosis (GRADS) Study. Sarcoidosis Protocol.
Survival in interstitial pneumonia with features of autoimmune disease: a comparison of proposed criteria.
The effect of bronchodilators on forced vital capacity measurement in patients with idiopathic pulmonary fibrosis.
Longitudinal analysis of sarcoidosis blood transcriptomic signatures and disease outcomes.
The WASOG Sarcoidosis Organ Assessment Instrument: An update of a previous clinical tool.
Surgical lung biopsy over bronchoalveolar lavage in chronic hypersensitivity pneumonitis.
Interferon-inducible chemokines reflect severity and progression in sarcoidosis.
Invariant natural killer T (iNKT) cell exhaustion in sarcoidosis.
Prevalence and prognosis of unclassifiable interstitial lung disease.
Sarcoidosis blood transcriptome reflects lung inflammation and overlaps with tuberculosis.
DAP12 is required for macrophage recruitment to the lung in response to cigarette smoke and chemotaxis toward CCL2.
T-helper type 2-driven inflammation defines major subphenotypes of asthma.
Integrin beta6 mediates phospholipid and collectin homeostasis by activation of latent TGF-beta1.
Idiopathic nonspecific interstitial pneumonia: lung manifestation of undifferentiated connective tissue disease?
A distinctive alveolar macrophage activation state induced by cigarette smoking.
Aspergillus antigen induces robust Th2 cytokine production, inflammation, airway hyperreactivity and fibrosis in the absence of MCP-1 or CCR2.
Hard metal interstitial lung disease: high-resolution computed tomography appearance.
Direct effects of interleukin-13 on epithelial cells cause airway hyperreactivity and mucus overproduction in asthma.
Interleukin-13 induces dramatically different transcriptional programs in three human airway cell types.
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