Beata Kośmider

ORCID: 0000-0001-7421-5424
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About
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Research Areas
  • Neonatal Respiratory Health Research
  • Chronic Obstructive Pulmonary Disease (COPD) Research
  • Metal complexes synthesis and properties
  • Respiratory Support and Mechanisms
  • Genomics, phytochemicals, and oxidative stress
  • Free Radicals and Antioxidants
  • Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
  • Synthesis and biological activity
  • Medical Imaging and Pathology Studies
  • Influenza Virus Research Studies
  • Congenital Diaphragmatic Hernia Studies
  • Inhalation and Respiratory Drug Delivery
  • Immune Response and Inflammation
  • RNA modifications and cancer
  • Carcinogens and Genotoxicity Assessment
  • Pediatric health and respiratory diseases
  • S100 Proteins and Annexins
  • Air Quality and Health Impacts
  • Synthesis of Organic Compounds
  • Epigenetics and DNA Methylation
  • DNA Repair Mechanisms
  • Atherosclerosis and Cardiovascular Diseases
  • Fibroblast Growth Factor Research
  • Adipokines, Inflammation, and Metabolic Diseases
  • Redox biology and oxidative stress

Temple University
2016-2024

Institut thématique Immunologie, inflammation, infectiologie et microbiologie
2023

National Jewish Health
2008-2019

University of Colorado Denver
2008-2019

Zero to Three
2019

Aarhus University
2014

Institut de Biologie du Développement Marseille
2014

Aix-Marseille Université
2014

University of Łódź
2004-2011

Texas A&M University System
2005-2007

Alveolar epithelium plays a pivotal role in protecting the lungs from inhaled infectious agents. Therefore, regenerative capacity of alveolar is critical for recovery these insults order to rebuild epithelial barrier and restore pulmonary functions. Here, we show that sublethal infection mice with Streptococcus pneumoniae, most common pathogen community-acquired pneumonia, led exclusive damage lung alveoli, followed by regeneration resolution inflammation. We surfactant protein C–expressing...

10.1172/jci125014 article EN Journal of Clinical Investigation 2019-04-14

Alveolar Type II (ATII) cells are important targets for seasonal and pandemic influenza. To investigate the influenza-induced innate immune response in those cells, we measured global gene expression profile of highly differentiated ATII infected with influenza A virus at a multiplicity infection 0.5 4 hours 24 after inoculation. Infection stimulated significant increase mRNA concentrations many host defense-related genes, including pattern/pathogen recognition receptors, IFN, IFN-induced...

10.1165/rcmb.2010-0108oc article EN American Journal of Respiratory Cell and Molecular Biology 2011-01-15

Angiogenesis, in which new blood vessels form via endothelial cell (EC) sprouting from existing vessels, is a critical event embryonic development and multiple disease processes. Many insights have been made into key EC receptors ligands/growth factors that govern angiogenesis, but intracellular molecular mechanisms of this process are not well understood. NF-E2-related factor 2 (Nrf2) transcription well-known for regulating the stress response pathologic settings, its role less appreciated....

10.1073/pnas.1309276110 article EN Proceedings of the National Academy of Sciences 2013-09-23

Background Cigarette smoke (CS) is a highly complex mixture and many of its components are known carcinogens, mutagens, other toxic substances. CS induces oxidative stress cell death, this toxicity plays key role in the pathogenesis several pulmonary diseases. Methodology/Principal Findings We studied effect cigarette extract (CSE) human alveolar epithelial type I-like (ATI-like) cells. These isolated II cells that differentiating toward I phenotype vitro have lost markers express markers....

10.1371/journal.pone.0026059 article EN cc-by PLoS ONE 2011-12-07

The alveolar surface is covered by an epithelium composed of 2 main cell types: type I and II cells. Alveolar (ATII) cells have a distinct morphology with apical microvilli characteristic lamellar bodies, which are the intracellular storage form pulmonary surfactant. ATII play important role in innate immunity produce secrete They proliferate to restore after damage more sensitive We developed efficient rapid method isolate purify from mice. epithelial were dissociated murine lung dispase...

10.3109/01902148.2012.713077 article EN Experimental Lung Research 2012-08-13

BackgroundCigarette smoke is the main risk factor of pulmonary emphysema development, which characterized by alveolar wall destruction. Mitochondria are important for type II (ATII) cell metabolism due to ATP generation.MethodsWe isolated ATII cells from control non-smoker and smoker organ donors, after lung transplant patients with determine mitochondrial function, dynamics (mt) DNA damage.FindingsWe found high superoxide generation mtDNA damage in emphysema. This correlated decreased...

10.1016/j.ebiom.2019.07.063 article EN cc-by-nc-nd EBioMedicine 2019-08-01

Electronic cigarette (e-cig) use has recently been implicated in promoting atherosclerosis. In this study, we aimed to investigate the mechanism of e-cig exposure accelerated atherosclerotic lesion development. Approach and Results: Eight-week-old ApoE-/- mice fed normal laboratory diet were exposed vapor (ECV) for 2 hours/day, 5 days/week 16 weeks. We found that ECV significantly induced lesions as examined by Oil Red O staining greatly upregulated TLR9 (toll-like receptor 9) expression...

10.1161/atvbaha.120.315556 article EN Arteriosclerosis Thrombosis and Vascular Biology 2020-12-31

Cigarette smoke (CS) is a main risk factor for chronic obstructive pulmonary disease (COPD). Oxidative stress induced by CS causes DNA and lung damage. Oxidant/antioxidant imbalance occurs in the distal air spaces of smokers patients with COPD. We studied effect oxidative generated both vivo vitro on murine primary alveolar type II (ATII) cells isolated from nuclear erythroid 2-related factor-2 (Nrf2)(-/-) mice. determined human ATII cell injury analyzed smoker non-smoker donors ex vivo....

10.1038/cddis.2013.96 article EN cc-by Cell Death and Disease 2013-04-04

Long-chain acyl-CoA dehydrogenase (LCAD) is a mitochondrial fatty acid oxidation enzyme whose expression in humans low or absent organs known to utilize acids for energy such as heart, muscle, and liver. This study demonstrates localization of LCAD human alveolar type II pneumocytes, which synthesize secrete pulmonary surfactant. The physiological role the pathway lung was subsequently studied using knock-out mice. Lung reduced LCAD−/− mice demonstrated compliance, but histological...

10.1074/jbc.m113.540260 article EN cc-by Journal of Biological Chemistry 2014-03-04

Rationale Alveolar type II (ATII) cells act as adult stem contributing to alveolar I (ATI) cell renewal and play a major role in idiopathic pulmonary fibrosis (IPF), supported by familial cases harbouring mutations genes specifically expressed these cells. During IPF, ATII lose their regenerative potential aberrantly express pathways epithelial–mesenchymal transition (EMT). The microRNA miR-200 family is downregulated but its effect on human IPF remains unproven. We wanted 1) evaluate the...

10.1183/23120541.00138-2019 article EN cc-by-nc ERJ Open Research 2019-10-01

Abstract Aging impairs the immune responses to influenza A virus (IAV), resulting in increased mortality IAV infections older adults. However, factors within aged lung that compromise host defense remain unknown. Using a murine model and human samples, we identified prostaglandin E 2 (PGE ), as such factor. Senescent type II alveolar epithelial cells (AECs) are overproducers of PGE lung. proliferation macrophages (AMs), critical for against respiratory pathogens, via reduction oxidative...

10.1038/s41467-022-34593-y article EN cc-by Nature Communications 2022-11-09

Lipids play a central role in lung physiology and pathology; however, comprehensive lipidomic characterization of human pulmonary cells relevant to disease has not been performed. The involved host defense, including alveolar macrophages (AMs), bronchial epithelial (BECs), type II (ATIIs), were isolated from subjects analysis by LC-MS LC-MS/MS was Additionally, pieces tissue the same donors analyzed MALDI imaging MS order determine lipid localization tissue. unique distribution phospholipids...

10.1194/jlr.m074955 article EN cc-by Journal of Lipid Research 2017-03-10

Emphysema is caused by the cigarette smoke (CS)-induced destruction of alveolar wall septa, and CS main risk factor for chronic obstructive pulmonary disease (COPD). To study mechanisms response to this insult, we focused on oxidant-induced lung injury potential role nuclear erythroid 2-related factor-2 (Nrf2), which a key regulator antioxidant defense system. We studied protective N-acetylcysteine (NAC) against type II (ATII) cells induced in vivo vitro. ATII were isolated purified using...

10.1165/rcmb.2012-0295oc article EN American Journal of Respiratory Cell and Molecular Biology 2013-03-15

Identification of biomarkers cigarette smoke -induced lung damage and early COPD is an area intense interest. Glucose regulated protein 78 kD (i.e., GRP78), a multi-functional which mediates cell responses to oxidant stress, increased in the lungs smokers serum subjects with COPD. We have suggested that secretion GRP78 by cells may explain increase To assess lung, we assayed bronchoalveolar lavage fluid (BALF) chronic non-smokers. also directly assessed acute effect material on isolated...

10.1186/s12931-017-0561-6 article EN cc-by Respiratory Research 2017-05-02
Parth Rali O.A. O’Corragain Lawrence Oresanya Daohai Yu Omar Sheriff and 95 more Robert A. Weiss C.N. Myers Parag Desai Nadia Ali Anthony Stack Michael Bromberg Andrea L. Lubitz J. Panaro Riyaz Bashir Vladimir Lakhter Roberto Caricchio Rohit Gupta Chandra Dass Maruti Kumaran Xiaoning Lu A. Koneti Rao Gary Cohen Gerard J. Criner Eric T. Choi Aaron Mishkin Abbas Abba Abhijit Pathak Abhinav Rastogi Adam Diamond Aditi Satti Adria Simon Ahmed M. Soliman Alan Braveman A.J. Mamary A. Pandya Amy J. Goldberg Amy Kambo A.J. Gangemi Anjali Vaidya Ann Davison Anuj Basil Beata Kośmider Charles Bakhos Bill Cornwell Brianna Sanguily Brittany Corso Carla Grabianowski Carly Sedlock C.N. Myers C.N. Myers Charles Bakhos Chenna Kesava Reddy Mandapati Cherie P. Erkmen Chethan Gangireddy Chih-Ru Lin Christopher T. Burks Claire Raab Deborah L. Crabbe Crystal Chen Daniel Edmundowicz D. Sacher Daniel Salerno Daniele Simon David M. Ambrose David Ciccolella Debra Gillman Dolores Fehrle Dominic Morano Donnalynn Bassler Edmund Cronin Eduardo Dominguez E.S. Randhawa Ekamjeet Randhawa Eman Hamad Eneida Male Erin Narewski Francis Cordova Frederic Jaffe Frederich Kueppers Fusun Dikengil Jonathan J. Galli A.J. Gangemi Jamie L. Garfield Gayle M Jones Gennaro Calendo Gerard J. Criner Gilbert E. D’Alonzo Ginny Marmolejos Matthew Gordon G. Millio Rohit Gupta Fernandez Gustavo Hannah Leah Tadeja Simborio Harwood Scott Heidi Shore-Brown H S Villanueva Alvarado Ho‐Man Yeung Ibraheem Yousef I. Oriaku Iris Jung-won Lee

Infection with the novel severe acute respiratory syndrome coronavirus 2 has been associated a hypercoagulable state. Emerging data from China and Europe have consistently shown an increased incidence of venous thromboembolism (VTE). We aimed to identify VTE early predictors at our high-volume tertiary care center.We performed retrospective cohort study 147 patients who had admitted Temple University Hospital disease 2019 (COVID-19) April 1, 2020 27, 2020. first identified (pulmonary...

10.1016/j.jvsv.2020.09.006 article EN publisher-specific-oa Journal of Vascular Surgery Venous and Lymphatic Disorders 2020-10-05

The early inflammatory response to influenza A virus infection contributes severe lung disease and continues pose a serious threat human health. mechanisms by which cells invade the respiratory tract remain unclear. Uncontrolled inflammation oxidative stress cause damage in infection. We have previously shown that fatty acid binding protein 5 (FABP5) has anti-inflammatory properties. speculate that, as transporter of acids, FABP5 plays an important protective role against lipids during well....

10.1152/ajplung.00276.2012 article EN AJP Lung Cellular and Molecular Physiology 2013-04-27

Cigarette smoke (CS) is a main source of oxidative stress and key risk factor for emphysema, which consists alveolar wall destruction. Alveolar type (AT) II cells are in the gas exchange regions lung. We isolated primary ATII from deidentified organ donors whose lungs were not suitable transplantation. analyzed cell injury obtained nonsmokers, moderate smokers, heavy smokers. DJ-1 protects induces nuclear erythroid 2-related factor-2 (Nrf2) expression, activates antioxidant defense system....

10.1165/rcmb.2015-0304oc article EN American Journal of Respiratory Cell and Molecular Biology 2016-04-19

Rationale: The association between non-tuberculous mycobacterial lung disease and alpha-1-antitrypsin (AAT) deficiency is likely due, in part, to underlying emphysema or bronchiectasis. But there increasing evidence that AAT itself enhances host immunity against microbial pathogens thus could compromise protection. Objectives: goal of this project determine if augment macrophage activity mycobacteria. Methods: We compared the ability monocyte-derived macrophages cultured autologous plasma...

10.3389/fimmu.2019.01417 article EN cc-by Frontiers in Immunology 2019-06-26
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