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Article ; Online: A no-Wnt situation for alveolar macrophage self-renewal.

Suber, Tomeka / Camiolo, Matthew J / Ray, Anuradha

2021 Volume 54, Issue 6, Page(s) 1099–1101

Abstract: Alveolar macrophages (AMs) are central to defense against respiratory pathogens. Impediments in restoring AMs after infection increase the risk for superinfection, which is associated with significant morbidity and mortality worldwide. In this issue of ... ...

Abstract	Alveolar macrophages (AMs) are central to defense against respiratory pathogens. Impediments in restoring AMs after infection increase the risk for superinfection, which is associated with significant morbidity and mortality worldwide. In this issue of Immunity, Zhu et al. report a Wnt-β-catenin-HIF-1α axis in AMs that promotes an inflammatory phenotype while restricting proliferation and self-renewal.
MeSH term(s)	Macrophages, Alveolar ; Phenotype
Language	English
Publishing date	2021-06-07
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2021.05.013
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Zs.A 4227: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 69: Show issues

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Article ; Online: Inclusion in the Pulmonary, Critical Care, and Sleep Medicine Physician-Scientist Workforce. Building with Intention.

Suber, Tomeka L / Neptune, Enid R / Lee, Janet S

ATS scholar

2020 Volume 1, Issue 4, Page(s) 353–363

Abstract: Physician-scientists comprise an exceedingly small fraction of the physician workforce. As the fields of pulmonary, critical care, and sleep medicine continue to invest in the development of the physician-scientist workforce, recruitment and retention ... ...

Abstract	Physician-scientists comprise an exceedingly small fraction of the physician workforce. As the fields of pulmonary, critical care, and sleep medicine continue to invest in the development of the physician-scientist workforce, recruitment and retention strategies need to consider the temporal trend in the decline in numbers of trainees pursuing basic research, the challenges of trainees from underrepresented groups in medicine, and opportunities for career and scientific advancement of women physician-scientists. In this perspective article, we examine the headwinds in the training and education of physician-scientists and highlight potential solutions to reverse these trends.
Language	English
Publishing date	2020-08-12
Publishing country	United States
Document type	Journal Article
ISSN	2690-7097
ISSN (online)	2690-7097
DOI	10.34197/ats-scholar.2020-0026PS
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Article ; Online: An Emerging Role for Megalin as a Regulator of Protein Leak in Acute Lung Injury.

Suber, Tomeka / Mallampalli, Rama K

American journal of respiratory cell and molecular biology

2017 Volume 57, Issue 5, Page(s) 504–505

MeSH term(s)	Acute Lung Injury/metabolism ; Acute Lung Injury/pathology ; Acute Lung Injury/therapy ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Humans ; Low Density Lipoprotein Receptor-Related Protein-2/metabolism ; Mice ; Mice, Knockout ; Respiratory Distress Syndrome/metabolism ; Respiratory Distress Syndrome/pathology ; Respiratory Distress Syndrome/therapy
Chemical Substances	Adaptor Proteins, Signal Transducing ; LRP2BP protein, human ; Low Density Lipoprotein Receptor-Related Protein-2
Language	English
Publishing date	2017-10-30
Publishing country	United States
Document type	Editorial
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2017-0224ED
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Zs.A 2851: Show issues

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Article: Glucocorticoid use in acute respiratory failure from pulmonary causes and association with early changes in the systemic host immune response.

Al-Yousif, Nameer / Nouraie, Seyed M / Broerman, Matthew J / Zhang, Yingze / Suber, Tomeka L / Evankovich, John / Bain, William G / Kitsios, Georgios D / McVerry, Bryan J / Shah, Faraaz A

Intensive care medicine experimental

2024 Volume 12, Issue 1, Page(s) 24

Abstract: Background: Glucocorticoids are commonly used in patients with or at-risk for acute respiratory distress syndrome (ARDS), but optimal use remains unclear despite well-conducted clinical trials. We performed a secondary analysis in patients previously ... ...

Abstract	Background: Glucocorticoids are commonly used in patients with or at-risk for acute respiratory distress syndrome (ARDS), but optimal use remains unclear despite well-conducted clinical trials. We performed a secondary analysis in patients previously enrolled in the Acute Lung Injury and Biospecimen Repository at the University of Pittsburgh. The primary aim of our study was to investigate early changes in host response biomarkers in response to real-world use of glucocorticoids in patients with acute respiratory failure due to ARDS or at-risk due to a pulmonary insult. Participants had baseline plasma samples obtained on study enrollment and on follow-up 3 to 5 days later to measure markers of innate immunity (IL-6, IL-8, IL-10, TNFr1, ST2, fractalkine), epithelial injury (sRAGE), endothelial injury (angiopoietin-2), and host response to bacterial infections (procalcitonin, pentraxin-3). In our primary analyses, we investigated the effect of receiving glucocorticoids between baseline and follow-up samples on host response biomarkers measured at follow-up by doubly robust inverse probability weighting analysis. In exploratory analyses, we examined associations between glucocorticoid use and previously characterized host response subphenotypes (hyperinflammatory and hypoinflammatory). Results: 67 of 148 participants (45%) received glucocorticoids between baseline and follow-up samples. Dose and type of glucocorticoids varied. Regimens that used hydrocortisone alone were most common (37%), and median daily dose was equivalent to 40 mg methylprednisolone (interquartile range: 21, 67). Participants who received glucocorticoids were more likely to be female, to be on immunosuppressive therapy at baseline, and to have higher baseline levels of ST-2, fractalkine, IL-10, pentraxin-3, sRAGE, and TNFr1. Glucocorticoid use was associated with decreases in IL-6 and increases in fractalkine. In exploratory analyses, glucocorticoid use was more frequent in participants in the hyperinflammatory subphenotype (58% vs 40%, p = 0.05), and was not associated with subphenotype classification at the follow-up time point (p = 0.16). Conclusions: Glucocorticoid use varied in a cohort of patients with or at-risk for ARDS and was associated with early changes in the systemic host immune response.
Language	English
Publishing date	2024-03-05
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2740385-3
ISSN	2197-425X
ISSN	2197-425X
DOI	10.1186/s40635-024-00605-y
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Article ; Online: Serum metabolomic signatures of fatty acid oxidation defects differentiate host-response subphenotypes of acute respiratory distress syndrome.

Suber, Tomeka L / Wendell, Stacy G / Mullett, Steven J / Zuchelkowski, Benjamin / Bain, William / Kitsios, Georgios D / McVerry, Bryan J / Ray, Prabir / Ray, Anuradha / Mallampalli, Rama K / Zhang, Yingze / Shah, Faraaz / Nouraie, Seyed Mehdi / Lee, Janet S

Respiratory research

2023 Volume 24, Issue 1, Page(s) 136

Abstract: Background: Fatty acid oxidation (FAO) defects have been implicated in experimental models of acute lung injury and associated with poor outcomes in critical illness. In this study, we examined acylcarnitine profiles and 3-methylhistidine as markers of ... ...

Abstract	Background: Fatty acid oxidation (FAO) defects have been implicated in experimental models of acute lung injury and associated with poor outcomes in critical illness. In this study, we examined acylcarnitine profiles and 3-methylhistidine as markers of FAO defects and skeletal muscle catabolism, respectively, in patients with acute respiratory failure. We determined whether these metabolites were associated with host-response ARDS subphenotypes, inflammatory biomarkers, and clinical outcomes in acute respiratory failure. Methods: In a nested case-control cohort study, we performed targeted analysis of serum metabolites of patients intubated for airway protection (airway controls), Class 1 (hypoinflammatory), and Class 2 (hyperinflammatory) ARDS patients (N = 50 per group) during early initiation of mechanical ventilation. Relative amounts were quantified by liquid chromatography high resolution mass spectrometry using isotope-labeled standards and analyzed with plasma biomarkers and clinical data. Results: Of the acylcarnitines analyzed, octanoylcarnitine levels were twofold increased in Class 2 ARDS relative to Class 1 ARDS or airway controls (P = 0.0004 and < 0.0001, respectively) and was positively associated with Class 2 by quantile g-computation analysis (P = 0.004). In addition, acetylcarnitine and 3-methylhistidine were increased in Class 2 relative to Class 1 and positively correlated with inflammatory biomarkers. In all patients within the study with acute respiratory failure, increased 3-methylhistidine was observed in non-survivors at 30 days (P = 0.0018), while octanoylcarnitine was increased in patients requiring vasopressor support but not in non-survivors (P = 0.0001 and P = 0.28, respectively). Conclusions: This study demonstrates that increased levels of acetylcarnitine, octanoylcarnitine, and 3-methylhistidine distinguish Class 2 from Class 1 ARDS patients and airway controls. Octanoylcarnitine and 3-methylhistidine were associated with poor outcomes in patients with acute respiratory failure across the cohort independent of etiology or host-response subphenotype. These findings suggest a role for serum metabolites as biomarkers in ARDS and poor outcomes in critically ill patients early in the clinical course.
MeSH term(s)	Humans ; Acetylcarnitine ; Case-Control Studies ; Biomarkers ; Respiratory Distress Syndrome/diagnosis ; Respiratory Insufficiency/diagnosis ; Respiratory Insufficiency/complications ; Fatty Acids
Chemical Substances	octanoylcarnitine (S1HB7P0O16) ; Acetylcarnitine (6DH1W9VH8Q) ; Biomarkers ; Fatty Acids
Language	English
Publishing date	2023-05-20
Publishing country	England
Document type	Journal Article
ZDB-ID	2041675-1
ISSN	1465-993X ; 1465-993X
ISSN (online)	1465-993X
ISSN	1465-993X
DOI	10.1186/s12931-023-02447-w
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Article: In vivo

Bain, William / Ahn, Brian / Peñaloza, Hernán F / McElheny, Christi L / Tolman, Nathanial / van der Geest, Rick / Gonzalez-Ferrer, Shekina / Chen, Nathalie / An, Xiaojing / Hosuru, Ria / Tabary, Mohammadreza / Papke, Erin / Kohli, Naina / Farooq, Nauman / Bachman, William / Olonisakin, Tolani F / Xiong, Zeyu / Griffith, Marissa P / Sullivan, Mara /

Franks, Jonathan / Mustapha, Mustapha M / Iovleva, Alina / Suber, Tomeka / Shanks, Robert Q / Ferreira, Viviana P / Stolz, Donna B / Van Tyne, Daria / Doi, Yohei / Lee, Janet S

bioRxiv : the preprint server for biology

2023

Abstract: Klebsiella ... ...

Abstract	Klebsiella pneumoniae
Language	English
Publishing date	2023-06-01
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.05.31.542722
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Article ; Online: In vivo evolution of a Klebsiella pneumoniae capsule defect with wcaJ mutation promotes complement-mediated opsono-phagocytosis during recurrent infection.

Franks, Jonathan / Mustapha, Mustapha M / Iovleva, Alina / Suber, Tomeka / Shanks, Robert Q / Ferreira, Viviana P / Stolz, Donna B / Van Tyne, Daria / Doi, Yohei / Lee, Janet S

The Journal of infectious diseases

2024

Abstract: Background: Klebsiella pneumoniae carbapenemase-producing K. pneumoniae (KPC-Kp) bloodstream infections are associated with high mortality. We studied clinical bloodstream KPC-Kp isolates to investigate mechanisms of resistance to complement, a key host ...

Abstract	Background: Klebsiella pneumoniae carbapenemase-producing K. pneumoniae (KPC-Kp) bloodstream infections are associated with high mortality. We studied clinical bloodstream KPC-Kp isolates to investigate mechanisms of resistance to complement, a key host defense against bloodstream infection. Methods: We tested growth of KPC-Kp isolates in human serum. In serial isolates from a single patient, we performed whole genome sequencing and tested for complement resistance and binding by mixing study, direct ELISA, flow cytometry, and electron microscopy. We utilized an isogenic deletion mutant in phagocytosis assays and an acute lung infection model. Results: We found serum resistance in 16 of 59 (27%) KPC-Kp clinical bloodstream isolates. In five genetically-related bloodstream isolates from a single patient, we noted a loss-of-function mutation in the capsule biosynthesis gene, wcaJ. Disruption of wcaJ was associated with decreased polysaccharide capsule, resistance to complement-mediated killing, and surprisingly, increased binding of complement proteins. Furthermore, an isogenic wcaJ deletion mutant exhibited increased opsono-phagocytosis in vitro and impaired in vivo control in the lung after airspace macrophage depletion in mice. Conclusions: Loss of function in wcaJ led to increased complement resistance, complement binding, and opsono-phagocytosis, which may promote KPC-Kp persistence by enabling co-existence of increased bloodstream fitness and reduced tissue virulence.
Language	English
Publishing date	2024-01-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	3019-3
ISSN	1537-6613 ; 0022-1899
ISSN (online)	1537-6613
ISSN	0022-1899
DOI	10.1093/infdis/jiae003
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Uh II Zs.50: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MO 445: Show issues

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Article ; Online: Lung Epithelium Releases Growth Differentiation Factor 15 in Response to Pathogen-mediated Injury.

Shah, Faraaz A / Bahudhanapati, Harinath / Jiang, Mao / Tabary, Mohammadreza / van der Geest, Rick / Tolman, Nathanial J / Kochin, Megan / Xiong, Zeyu / Al-Yousif, Nameer / Sayed, Khaled / Benos, Panayiotis V / Raffensperger, Kristen / Evankovich, John / Neal, Matthew D / Snyder, Mark E / Eickelberg, Oliver / Ray, Prabir / Dela Cruz, Charles / Bon, Jessica /

McVerry, Bryan J / Straub, Adam C / Jurczak, Michael J / Suber, Tomeka L / Zhang, Yingze / Chen, Kong / Kitsios, Georgios D / Lee, Janet S / Alder, Jonathan K / Bain, William G

American journal of respiratory cell and molecular biology

2024 Volume 70, Issue 5, Page(s) 379–391

Abstract: GDF15 (growth differentiation factor 15) is a stress cytokine with several proposed roles, including support of stress erythropoiesis. Higher circulating GDF15 levels are prognostic of mortality during acute respiratory distress syndrome, but the ... ...

Abstract	GDF15 (growth differentiation factor 15) is a stress cytokine with several proposed roles, including support of stress erythropoiesis. Higher circulating GDF15 levels are prognostic of mortality during acute respiratory distress syndrome, but the cellular sources and downstream effects of GDF15 during pathogen-mediated lung injury are unclear. We quantified GDF15 in lower respiratory tract biospecimens and plasma from patients with acute respiratory failure. Publicly available data from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection were reanalyzed. We used mouse models of hemorrhagic acute lung injury mediated by
MeSH term(s)	Growth Differentiation Factor 15/genetics ; Growth Differentiation Factor 15/metabolism ; Animals ; COVID-19/metabolism ; COVID-19/virology ; Humans ; Mice ; SARS-CoV-2 ; Pseudomonas aeruginosa ; Lung/metabolism ; Lung/pathology ; Lung/virology ; Male ; Pseudomonas Infections/metabolism ; Acute Lung Injury/pathology ; Acute Lung Injury/metabolism ; Female ; Mice, Inbred C57BL ; Mice, Knockout ; Respiratory Mucosa/metabolism ; Respiratory Mucosa/pathology ; Disease Models, Animal
Chemical Substances	Growth Differentiation Factor 15 ; GDF15 protein, human ; Gdf15 protein, mouse
Language	English
Publishing date	2024-02-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2023-0429OC
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Article ; Online: Considerations for Racial Diversity in the Cardiology Workforce in the United States of America.

Johnson, Amber E / Birru Talabi, Mehret / Bonifacino, Eliana / Culyba, Alison J / Jonassaint, Naudia L / Nance, Melonie A / Napoé, G Sarah / Olafiranye, Oladipupo / Owusu-Ansah, Sylvia / Suber, Tomeka L

Journal of the American College of Cardiology

2021 Volume 77, Issue 15, Page(s) 1934–1937

MeSH term(s)	Cardiology/statistics & numerical data ; Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/ethnology ; Cardiovascular Diseases/therapy ; Continental Population Groups/statistics & numerical data ; Cultural Competency ; Cultural Diversity ; Ethnic Groups/statistics & numerical data ; Health Workforce/statistics & numerical data ; Humans ; Population Groups/statistics & numerical data ; United States/epidemiology
Language	English
Publishing date	2021-04-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	605507-2
ISSN	1558-3597 ; 0735-1097
ISSN (online)	1558-3597
ISSN	0735-1097
DOI	10.1016/j.jacc.2021.02.043
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Zs.A 1846: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 196: Show issues

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Article ; Online: AM966, an Antagonist of Lysophosphatidic Acid Receptor 1, Increases Lung Microvascular Endothelial Permeability through Activation of Rho Signaling Pathway and Phosphorylation of VE-Cadherin.

Cai, Junting / Wei, Jianxin / Li, Shuang / Suber, Tomeka / Zhao, Jing

Mediators of inflammation

2017 Volume 2017, Page(s) 6893560

Abstract: Maintenance of pulmonary endothelial barrier integrity is important for reducing severity of lung injury. Lysophosphatidic acid (LPA) regulates cell motility, cytoskeletal rearrangement, and cell growth. Knockdown of LPA receptor 1 (LPA1) has been shown ... ...

Abstract	Maintenance of pulmonary endothelial barrier integrity is important for reducing severity of lung injury. Lysophosphatidic acid (LPA) regulates cell motility, cytoskeletal rearrangement, and cell growth. Knockdown of LPA receptor 1 (LPA1) has been shown to mitigate lung injury and pulmonary fibrosis. AM966, an LPA1 antagonist exhibiting an antifibrotic property, has been considered to be a future antifibrotic medicine. Here, we report an unexpected effect of AM966, which increases lung endothelial barrier permeability. An electric cell-substrate sensing (ECIS) system was used to measure permeability in human lung microvascular endothelial cells (HLMVECs). AM966 decreased the transendothelial electrical resistance (TEER) value immediately in a dose-dependent manner. VE-cadherin and f-actin double immunostaining reveals that AM966 increases stress fibers and gap formation between endothelial cells. AM966 induced phosphorylation of myosin light chain (MLC) through activation of RhoA/Rho kinase pathway. Unlike LPA treatment, AM966 had no effect on phosphorylation of extracellular signal-regulated kinases (Erk). Further, in LPA1 silencing cells, we observed that AM966-increased lung endothelial permeability as well as phosphorylation of VE-cadherin and focal adhesion kinase (FAK) were attenuated. This study reveals that AM966 induces lung endothelial barrier dysfunction, which is regulated by LPA1-mediated activation of RhoA/MLC and phosphorylation of VE-cadherin.
MeSH term(s)	Antigens, CD/metabolism ; Cadherins/metabolism ; Capillary Permeability/drug effects ; Carbamates/pharmacology ; Cell Line ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Focal Adhesion Protein-Tyrosine Kinases/metabolism ; Humans ; Lung/blood supply ; Phenylacetates/pharmacology ; Phosphorylation/drug effects ; Receptors, Lysophosphatidic Acid/antagonists & inhibitors ; Receptors, Lysophosphatidic Acid/metabolism ; Signal Transduction/drug effects ; rhoA GTP-Binding Protein/metabolism
Chemical Substances	(4'-(4-(1-(2-chlorophenyl)ethoxycarbonylamino)-3-methylisoxazol-5-yl)biphenyl-4-yl)acetic acid ; Antigens, CD ; Cadherins ; Carbamates ; Phenylacetates ; Receptors, Lysophosphatidic Acid ; cadherin 5 ; Focal Adhesion Protein-Tyrosine Kinases (EC 2.7.10.2) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; rhoA GTP-Binding Protein (EC 3.6.5.2)
Language	English
Publishing date	2017-02-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	1137605-3
ISSN	1466-1861 ; 0962-9351
ISSN (online)	1466-1861
ISSN	0962-9351
DOI	10.1155/2017/6893560
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