Faculty Bibliography
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36
Lung Microbiota Influence Responses to Anti-PD1 Therapy in a Preclinical Model of Non-small Cell Lung Cancer [Meeting Abstract]
ISI:001277613403475
ISSN: 1073-449x
CID: 5963522
Disease Phenotype in Bronchiectasis (NTM- and NTM plus ) Is Associated With Lower Airway Dysbiosis and Neutrophil Extracellular Traps [Meeting Abstract]
ISI:001277228900033
ISSN: 1073-449x
CID: 5963482
CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
ISI:001347342200014
ISSN: 1055-9965
CID: 5887122
American journal of respiratory & critical care medicine. 2023:208(10):1101-1114.DOI: 10.1164/rccm.202210-1865OC
Lower Airway Dysbiosis Augments Lung Inflammatory Injury in Mild-to-Moderate Chronic Obstructive Pulmonary Disease
PMID: 37677136
ISSN: 1535-4970
CID: 5606572
TGFβ-2 Haploinsufficiency Causes Early Death in Mice with Marfan Syndrome
To assess the contribution of individual TGF-β isoforms to aortopathy in Marfan syndrome (MFS), we quantified the survival and phenotypes of mice with a combined fibrillin1 (the gene defective in MFS) hypomorphic mutation and a TGF-β1, 2, or 3 heterozygous null mutation. The loss of TGF-β2, and only TGF-β2, resulted in 80% of the double mutant animals dying earlier, by post-natal day 20, than MFS only mice. Death was not from thoracic aortic rupture, as observed in MFS mice, but was associated with hyperplastic aortic valve leaflets, aortic regurgitation, enlarged aortic root, increased heart weight, and impaired lung alveolar septation. Thus, there appears to be a relationship between loss of fibrillin1 and TGF-β2 in the post-natal development of the heart, aorta and lungs.
PMID: 37217119
ISSN: 1569-1802
CID: 5543662
American journal of respiratory & critical care medicine. 2023:A2656-A2656.DOI: doi:10.1164/ajrccm-conference.2023.207.1_MeetingAbstracts.A2656
Complexities of the Lower Airway Microbiome in Bronchiectasis and NTM Lung Disease
ORIGINAL:0017181
ISSN: 1073-449x
CID: 5651622
American journal of respiratory cell & molecular biology. 2023:68(5):523-536.DOI: 10.1165/rcmb.2022-0269OC
Hedgehog and PDGF Signaling Intersect During Postnatal Lung Development
Normal lung development critically depends on Hedgehog (HH) and Platelet-derived growth factor (PDGF) signaling, which coordinate mesenchymal differentiation and proliferation. PDGF signaling is required for postnatal alveolar septum formation by myofibroblasts. Recently, we demonstrated a requirement for HH in postnatal lung development involving alveolar myofibroblast differentiation. Given shared features of HH and PDGF signaling and their impact/convergence on this key cell type, we sought to clarify their relationship during murine postnatal lung development. Timed experiments revealed that HH inhibition phenocopies the key lung myofibroblast phenotypes of Pdgfa and Pdgfra knockouts during secondary alveolar septation. Utilizing a dual signaling reporter, Gli1IZ;PdgfraEGFP
PMID: 36693140
ISSN: 1535-4989
CID: 5419542
Behcet's disease risk-variant HLA-B51/ERAP1-Hap10 alters human CD8 T cell immunity
OBJECTIVES/OBJECTIVE:, the classical risk factor for the disease. The mechanistic implications and biological consequences of this epistatic relationship are unknown. Here, we aimed to determine its biological relevance and functional impact. METHODS:LCL, analysed the HLA class I-bound peptidome for peptide length differences and assessed immunogenicity of genome-edited cells in CD8 T cell co-culture systems. RESULTS:KO cells showed peptidomes with longer peptides above 9mer and significant differences in their ability to stimulate alloreactive CD8 T cells compared with wild-type control cells. CONCLUSIONS:at the cellular level and point to an HLA-B51-restricted process. Our findings suggest that variant ERAP1-Hap10 partakes in BD pathogenesis by generating HLA-B51-restricted peptides, causing a change in immunodominance of the ensuing CD8 T cell response.
PMID: 35922122
ISSN: 1468-2060
CID: 5288102
Gpr125 is a unifying hallmark of multiple mammary progenitors coupled to tumor latency
Gpr125 is an orphan G-protein coupled receptor, with homology to cell adhesion and axonal guidance factors, that is implicated in planar polarity and control of cell movements. By lineage tracing we demonstrate that Gpr125 is a highly specific marker of bipotent mammary stem cells in the embryo and of multiple long-lived unipotent basal mammary progenitors in perinatal and postnatal glands. Nipple-proximal Gpr125+ cells express a transcriptomic profile indicative of chemo-repulsion and cell movement, whereas Gpr125+ cells concentrated at invasive ductal tips display a hybrid epithelial-mesenchymal phenotype and are equipped to bind chemokine and growth factors and secrete a promigratory matrix. Gpr125 progenitors acquire bipotency in the context of transplantation and cancer and are greatly expanded and massed at the pushing margins of short latency MMTV-Wnt1 tumors. High Gpr125 expression identifies patients with particularly poor outcome within the basal breast cancer subtype highlighting its potential utility as a factor to stratify risk.
PMID: 35302059
ISSN: 2041-1723
CID: 5181672
COVID-19 and Respiratory System Disorders: Current Knowledge, Future Clinical, and Translational Research Questions
The severe acute respiratory syndrome coronavirus-2 emerged as a serious human pathogen in late 2019, causing the disease coronavirus disease 2019 (COVID-19). The most common clinical presentation of severe COVID-19 is acute respiratory failure consistent with the acute respiratory distress syndrome. Airway, lung parenchymal, pulmonary vascular, and respiratory neuromuscular disorders all feature in COVID-19. This article reviews what is known about the effects of severe acute respiratory syndrome coronavirus-2 infection on different parts of the respiratory system, clues to understanding the underlying biology of respiratory disease, and highlights current and future translation and clinical research questions.
PMID: 32960072
ISSN: 1524-4636
CID: 4605602
