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Article ; Online: Molecular diagnostics for CLAD: When and where?

Greenland, John R / McDyer, John F

American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons

2022 Volume 22, Issue 4, Page(s) 1012–1013

MeSH term(s)	Allografts ; Bronchiolitis Obliterans ; Graft Rejection ; Humans ; Lung ; Lung Transplantation ; Pathology, Molecular
Language	English
Publishing date	2022-01-05
Publishing country	United States
Document type	Editorial ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	2060594-8
ISSN	1600-6143 ; 1600-6135
ISSN (online)	1600-6143
ISSN	1600-6135
DOI	10.1111/ajt.16925
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Article ; Online: Alveolar macrophage subsets: Accessories to lung alloimmune rejection.

Snyder, Mark E / McDyer, John F

The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation

2022 Volume 41, Issue 11, Page(s) 1570–1571

MeSH term(s)	Humans ; Macrophages, Alveolar ; Lung ; Lung Transplantation ; Graft Rejection
Language	English
Publishing date	2022-08-20
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	1062522-7
ISSN	1557-3117 ; 1053-2498
ISSN (online)	1557-3117
ISSN	1053-2498
DOI	10.1016/j.healun.2022.08.008
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Article ; Online: Single center study investigating the clinical association of donor-derived cell-free DNA with acute outcomes in lung transplantation

Kentaro Noda / Mark E. Snyder / Qingyong Xu / David Peters / John F. McDyer / Adriana Zeevi / Pablo G. Sanchez

Frontiers in Transplantation, Vol

2024 Volume 2

Abstract: BackgroundCirculating donor-derived cell-free DNA (dd-cfDNA) levels have been proposed as a potential tool for the diagnosis of graft injury. In this study, we prospectively investigated dd-cfDNA plasma levels and their association with severe primary ... ...

Abstract	BackgroundCirculating donor-derived cell-free DNA (dd-cfDNA) levels have been proposed as a potential tool for the diagnosis of graft injury. In this study, we prospectively investigated dd-cfDNA plasma levels and their association with severe primary graft dysfunction (PGD) and graft rejection after lung transplant.MethodsA total of 40 subjects undergoing de-novo lung transplants at our institution were recruited in this study. Blood samples were collected at various time points before and after lung transplant for 1 year. Dd-cfDNA in samples was determined using AlloSure assay (CareDx Inc.). The correlation of the value of %dd-cfDNA was investigated with the incidence of PGD, acute cellular rejection (ACR), and donor-specific antibody.ResultsWe observed a rapid increase of %dd-cfDNA in the blood of recipients after lung transplantation compared to baseline. The levels of dd-cfDNA decreased during the first two weeks. The peak was observed within 72 h after transplantation. The peak values of %dd-cfDNA varied among subjects and did not correlate with severe PGD incidence. We observed an association between levels of %dd-cfDNA from blood collected at the time of transbronchial biopsy and the histological diagnosis of ACR at 3 weeks.ConclusionOur data show that circulating dd-cfDNA levels are associated with ACR early after transplantation but not with severe PGD. Plasma levels of dd-cfDNA may be a less invasive tool to estimate graft rejection after lung transplantation however larger studies are still necessary to better identify thresholds.
Keywords	lung transplantation ; donor-derived cell-free DNA ; primary grafts dysfunction ; acute cellular rejection ; antibody-mediated rejection ; Specialties of internal medicine ; RC581-951
Subject code	610
Language	English
Publishing date	2024-01-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
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Article ; Online: Human telomere length is chromosome end-specific and conserved across individuals.

Karimian, Kayarash / Groot, Aljona / Huso, Vienna / Kahidi, Ramin / Tan, Kar-Tong / Sholes, Samantha / Keener, Rebecca / McDyer, John F / Alder, Jonathan K / Li, Heng / Rechtsteiner, Andreas / Greider, Carol W

Science (New York, N.Y.)

2024 , Page(s) eado0431

Abstract: Short telomeres cause age-related disease and long telomeres predispose to cancer; however, the mechanisms regulating telomere length are unclear. We developed a nanopore-based method, Telomere Profiling, to determine telomere length at nearly single ... ...

Abstract	Short telomeres cause age-related disease and long telomeres predispose to cancer; however, the mechanisms regulating telomere length are unclear. We developed a nanopore-based method, Telomere Profiling, to determine telomere length at nearly single nucleotide resolution. Mapping telomere reads to chromosome ends showed chromosome end-specific length distributions that could differ by more than six kilobases. Telomere lengths in 147 individuals showed certain chromosome ends were consistently longer or shorter. The same rank order was found in newborn cord blood, suggesting that telomere length is determined at birth and chromosome end-specific telomere length differences are maintained as telomeres shorten with age. Telomere Profiling makes precision investigation of telomere length widely accessible for laboratory, clinical, and drug discovery efforts and will allow deeper insights into telomere biology.
Language	English
Publishing date	2024-04-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	128410-1
ISSN	1095-9203 ; 0036-8075
ISSN (online)	1095-9203
ISSN	0036-8075
DOI	10.1126/science.ado0431
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Zs.A 27: 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)
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Article ; Online: SARS-CoV-2 Accessory Protein Orf7b Induces Lung Injury via c-Myc Mediated Apoptosis and Ferroptosis.

Deshpande, Rushikesh / Li, Wangyang / Li, Tiao / Fanning, Kristen V / Clemens, Zachary / Nyunoya, Toru / Zhang, Lianghui / Deslouches, Berthony / Barchowsky, Aaron / Wenzel, Sally / McDyer, John F / Zou, Chunbin

International journal of molecular sciences

2024 Volume 25, Issue 2

Abstract: The pandemic of coronavirus disease 2019 (COVID-19) has been the foremost modern global public health challenge. The airway is the primary target in severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2) infection, with substantial cell ... ...

Abstract	The pandemic of coronavirus disease 2019 (COVID-19) has been the foremost modern global public health challenge. The airway is the primary target in severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2) infection, with substantial cell death and lung injury being signature hallmarks of exposure. The viral factors that contribute to cell death and lung injury remain incompletely understood. Thus, this study investigated the role of open reading frame 7b (Orf7b), an accessory protein of the virus, in causing lung injury. In screening viral proteins, we identified Orf7b as one of the major viral factors that mediates lung epithelial cell death. Overexpression of Orf7b leads to apoptosis and ferroptosis in lung epithelial cells, and inhibitors of apoptosis and ferroptosis ablate Orf7b-induced cell death. Orf7b upregulates the transcription regulator, c-Myc, which is integral in the activation of lung cell death pathways. Depletion of c-Myc alleviates both apoptotic and ferroptotic cell deaths and lung injury in mouse models. Our study suggests a major role of Orf7b in the cell death and lung injury attributable to COVID-19 exposure, supporting it as a potential therapeutic target.
MeSH term(s)	Animals ; Mice ; Apoptosis ; COVID-19 ; Ferroptosis ; Lung Injury/virology ; Open Reading Frames ; SARS-CoV-2 ; Viral Proteins/genetics
Chemical Substances	ORF7b protein, SARS-CoV-2 ; Viral Proteins
Language	English
Publishing date	2024-01-18
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms25021157
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Article: Human telomere length is chromosome specific and conserved across individuals.

bioRxiv : the preprint server for biology

2024

Abstract: Short telomeres cause age-related disease and long telomeres predispose to cancer; however, the mechanisms regulating telomere length are unclear. To probe these mechanisms, we developed a nanopore sequencing method, Telomere Profiling, that is easy to ... ...

Abstract	Short telomeres cause age-related disease and long telomeres predispose to cancer; however, the mechanisms regulating telomere length are unclear. To probe these mechanisms, we developed a nanopore sequencing method, Telomere Profiling, that is easy to implement, precise, and cost effective with broad applications in research and the clinic. We sequenced telomeres from individuals with short telomere syndromes and found similar telomere lengths to the clinical FlowFISH assay. We mapped telomere reads to specific chromosome end and identified both chromosome end-specific and haplotype-specific telomere length distributions. In the T2T HG002 genome, where the average telomere length is 5kb, we found a remarkable 6kb difference in lengths between some telomeres. Further, we found that specific chromosome ends were consistently shorter or longer than the average length across 147 individuals. The presence of conserved chromosome end-specific telomere lengths suggests there are new paradigms in telomere biology that are yet to be explored. Understanding the mechanisms regulating length will allow deeper insights into telomere biology that can lead to new approaches to disease.
Language	English
Publishing date	2024-01-13
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.12.21.572870
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Article ; Online: Foxp3+ T lymphocytes: immune regulators within the lung allograft.

Lendermon, Elizabeth A / McDyer, John F

The Journal of clinical investigation

2018 Volume 129, Issue 2, Page(s) 494–495

Abstract: Antibody-mediated rejection (AMR) has emerged as an important cause of lung graft failure. In the current issue of the JCI, a study by Li et al. identifies a critical role of Foxp3+ T cells residing within lung allografts in the regulation of AMR. This ... ...

Abstract	Antibody-mediated rejection (AMR) has emerged as an important cause of lung graft failure. In the current issue of the JCI, a study by Li et al. identifies a critical role of Foxp3+ T cells residing within lung allografts in the regulation of AMR. This study not only provides new insights into the nature of lung allografts as a primary site where T and B cell priming and immune regulation can occur, but also introduces the mouse orthotopic lung transplant as a model for studying the immunobiology of AMR. Because AMR can be so difficult to effectively treat in lung transplant recipients, the development of an animal model is a major advance in understanding the immunopathogenesis of AMR.
MeSH term(s)	Allografts ; Animals ; Bronchi ; Forkhead Transcription Factors ; Graft Rejection ; Lung ; Lymphoid Tissue ; Mice ; T-Lymphocytes
Chemical Substances	Forkhead Transcription Factors ; Foxp3 protein, mouse
Language	English
Publishing date	2018-12-18
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI126517
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Ua VI Zs.184: Show issues

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Article ; Online: Incidence of Acute Cellular Rejection After Granulocyte Colony-Stimulating Factor in Lung Transplant Recipients.

Fredrick, Stacy R / Iasella, Carlo J / Sacha, Lauren M / Rivosecchi, Ryan M / Morrell, Matthew R / Sanchez, Pablo G / Pilewski, Joseph M / Snyder, Mark E / McDyer, John F / Moore, Cody A

Journal of pharmacy practice

2023 , Page(s) 8971900231184308

Abstract: BackgroundNeutropenia is a common complication in lung transplant recipients (LTRs). Filgrastim may be used to treat neutropenia in LTRs, but its consequences on acute cellular rejection (ACR) remain controversial. ...

Abstract	BackgroundNeutropenia is a common complication in lung transplant recipients (LTRs). Filgrastim may be used to treat neutropenia in LTRs, but its consequences on acute cellular rejection (ACR) remain controversial.
Language	English
Publishing date	2023-06-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	1027474-1
ISSN	1531-1937 ; 0897-1900
ISSN (online)	1531-1937
ISSN	0897-1900
DOI	10.1177/08971900231184308
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Zs.A 2893: Show issues

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Article ; Online: Pseudomonas-dominant microbiome elicits sustained IL-1β upregulation in alveolar macrophages from lung transplant recipients.

Britton, Noel / Villabona-Rueda, Andres / Whiteside, Samantha A / Mathew, Joby / Kelley, Matthew / Agbor-Enoh, Sean / McDyer, John F / Christie, Jason D / Collman, Ronald G / Cox, Andrea L / Shah, Pali / D'Alessio, Franco

The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation

2023 Volume 42, Issue 9, Page(s) 1166–1174

Abstract: Background: Isolation of Pseudomonas aeruginosa (PsA) is associated with increased BAL (bronchoalveolar lavage) inflammation and lung allograft injury in lung transplant recipients (LTR). However, the effect of PsA on macrophage responses in this ... ...

Abstract	Background: Isolation of Pseudomonas aeruginosa (PsA) is associated with increased BAL (bronchoalveolar lavage) inflammation and lung allograft injury in lung transplant recipients (LTR). However, the effect of PsA on macrophage responses in this population is incompletely understood. We examined human alveolar macrophage (AMΦ) responses to PsA and Pseudomonas dominant microbiome in healthy LTR. Methods: We stimulated THP-1 derived macrophages (THP-1MΦ) and human AMΦ from LTR with different bacteria and LTR BAL derived microbiome characterized as Pseudomonas-dominant. Macrophage responses were assessed by high dimensional flow cytometry, including their intracellular production of cytokines (TNF-α, IL-6, IL-8, IL-1β, IL-10, IL-1RA, and TGF-β). Pharmacological inhibitors were utilized to evaluate the role of the inflammasome in PsA-macrophage interaction. Results: We observed upregulation of pro-inflammatory cytokines (TNF-α, IL-6, IL-8, IL-1β) following stimulation by PsA compared to other bacteria (Staphylococcus aureus (S.Aur), Prevotella melaninogenica, Streptococcus pneumoniae) in both THP-1MΦ and LTR AMΦ, predominated by IL-1β. IL-1β production from THP-1MΦ was sustained after PsA stimulation for up to 96 hours and 48 hours in LTR AMΦ. Treatment with the inflammasome inhibitor BAY11-7082 abrogated THP-1MΦ IL-1β production after PsA exposure. BAL Pseudomonas-dominant microbiota elicited an increased IL-1β, similar to PsA, an effect abrogated by the addition of antibiotics. Conclusion: PsA and PsA-dominant lung microbiota induce sustained IL-1β production in LTR AMΦ. Pharmacological targeting of the inflammasome reduces PsA-macrophage-IL-1β responses, underscoring their use in lung transplant recipients.
MeSH term(s)	Humans ; Macrophages, Alveolar/metabolism ; Tumor Necrosis Factor-alpha ; Interleukin-6 ; Interleukin-8/metabolism ; Up-Regulation ; Pseudomonas/metabolism ; Inflammasomes ; Transplant Recipients ; Arthritis, Psoriatic ; Lung/metabolism ; Cytokines/metabolism
Chemical Substances	Tumor Necrosis Factor-alpha ; Interleukin-6 ; Interleukin-8 ; Inflammasomes ; Cytokines
Language	English
Publishing date	2023-04-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	1062522-7
ISSN	1557-3117 ; 1053-2498
ISSN (online)	1557-3117
ISSN	1053-2498
DOI	10.1016/j.healun.2023.04.005
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Article ; Online: Rabbit Antithymocyte Globulin for Treatment of Corticosteroid Refractory Acute Cellular Rejection After Lung Transplantation.

Rudzik, Katelyn N / Moore, Cody A / Sacha, Lauren M / Rivosecchi, Ryan M / Saul, Melissa / Pilewski, Joseph M / Kilaru, Silpa D / Snyder, Mark E / McDyer, John F / Iasella, Carlo J

Transplantation

2023 Volume 107, Issue 8, Page(s) 1828–1834

Abstract: Background: Chronic lung allograft dysfunction (CLAD) remains a major cause of death after the first year posttransplant, with acute cellular rejection (ACR) being a major risk factor for CLAD. We evaluated the use of rabbit antithymocyte globulin (rATG) ...

Abstract	Background: Chronic lung allograft dysfunction (CLAD) remains a major cause of death after the first year posttransplant, with acute cellular rejection (ACR) being a major risk factor for CLAD. We evaluated the use of rabbit antithymocyte globulin (rATG) for corticosteroid refractory ACR in lung transplant recipients. Methods: We retrospectively identified 112 adult lung transplant recipients who received rATG for refractory ACR after lung transplantation. The primary endpoint was the incidence of ACR on follow-up transbronchial biopsy. Secondary endpoints included freedom from ACR within 1 y post-rATG, CLAD progression at 1 y post-rATG, and all-cause mortality at 1 y post-rATG. Results: A complete resolution of ACR was observed in 60.2% of patients, an improvement but not complete resolution in 22.1%, and no response on follow-up biopsy in 17.8%. Mean A grade 1 y post-rATG was 0.51 in complete responders, 1.01 in partial responders, and 2.19 in nonresponders ( P < 0.001). Complete responders had significantly less new or worsening CLAD at 1 y than partial responders (17% versus 40%; P = 0.02). All-cause mortality rate was 14.9% in complete responders, 40% in partial responders, and 30% in nonresponders ( P < 0.01). Conclusions: rATG appears to be an effective treatment of refractory ACR in lung transplant recipients. Failure to respond to rATG carries an increased risk of early CLAD and death.
MeSH term(s)	Immunosuppressive Agents/adverse effects ; Retrospective Studies ; Antilymphocyte Serum/therapeutic use ; Adrenal Cortex Hormones/therapeutic use ; Lung Transplantation/adverse effects ; Graft Rejection/etiology
Chemical Substances	thymoglobulin (D7RD81HE4W) ; Immunosuppressive Agents ; Antilymphocyte Serum ; Adrenal Cortex Hormones
Language	English
Publishing date	2023-07-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	208424-7
ISSN	1534-6080 ; 0041-1337
ISSN (online)	1534-6080
ISSN	0041-1337
DOI	10.1097/TP.0000000000004617
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