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623 results on '"Kreisel, Daniel"'

3. CCR2 imaging in human ST-segment elevation myocardial infarction

Author

Lavine, Kory J., Sultan, Deborah, Luehmann, Hannah, Detering, Lisa, Zhang, Xiaohui, Heo, Gyu Seong, Zhang, Xiuli, Hoelscher, Michelle, Harrison, Kitty, Combadière, Christophe, Laforest, Richard, Kreisel, Daniel, Woodard, Pamela K., Brody, Steven L., Gropler, Robert J., and Liu, Yongjian

Published
2023
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9. The 2022 Banff Meeting Lung Report

Author

Pavlisko, Elizabeth N., Adam, Benjamin A., Berry, Gerald J., Calabrese, Fiorella, Cortes-Santiago, Nahir, Glass, Carolyn H., Goddard, Martin, Greenland, John R., Kreisel, Daniel, Levine, Deborah J., Martinu, Tereza, Verleden, Stijn E., Weigt, S. Sam, and Roux, Antoine

Published
2024
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10. B cells mediate lung ischemia/reperfusion injury by recruiting classical monocytes via synergistic B cell receptor/TLR4 signaling

Author

Farahnak, Khashayar, Bai, Yun Zhu, Yokoyama, Yuhei, Morkan, Deniz B., Liu, Zhiyi, Amrute, Junedh M., De Filippis Falcon, Alejandro, Terada, Yuriko, Liao, Fuyi, Li, Wenjun, Shepherd, Hailey M., Hachem, Ramsey R., Puri, Varun, Lavine, Kory J., Gelman, Andrew E., Bharat, Ankit, Kreisel, Daniel, and Nava, Ruben G.

Subjects
Thermo Fisher Scientific Inc., Transplantation of organs, tissues, etc., Medical research, Medicine, Experimental, Scientific equipment and supplies industry, Lung diseases, Immune response, B cells, Health care industry, Washington University. School of Medicine
Abstract

Ischemia/reperfusion injury-mediated (IRI-mediated) primary graft dysfunction (PGD) adversely affects both short- and long-term outcomes after lung transplantation, a procedure that remains the only treatment option for patients suffering from end-stage respiratory failure. While B cells are known to regulate adaptive immune responses, their role in lung IRI is not well understood. Here, we demonstrated by intravital imaging that B cells are rapidly recruited to injured lungs, where they extravasate into the parenchyma. Using hilar clamping and transplant models, we observed that lung-infiltrating B cells produce the monocyte chemokine CCL7 in a TLR4-TRIF-dependent fashion, a critical step contributing to classical monocyte (CM) recruitment and subsequent neutrophil extravasation, resulting in worse lung function. We found that synergistic BCR-TLR4 activation on B cells is required for the recruitment of CMs to the injured lung. Finally, we corroborated our findings in reperfused human lungs, in which we observed a correlation between B cell infiltration and CM recruitment after transplantation. This study describes a role for B cells as critical orchestrators of lung IRI. As B cells can be depleted with currently available agents, our study provides a rationale for clinical trials investigating B cell-targeting therapies., Introduction Primary graft dysfunction (PGD) is a common early complication after lung transplantation that adversely affects both shortand long-term outcomes. This includes both early morbidity and mortality as well as [...]

Published
2024
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13. Smoking exposure-induced bronchus-associated lymphoid tissue in donor lungs does not prevent tolerance induction after transplantation

Author

Terada, Yuriko, Li, Wenjun, Shepherd, Hailey M., Takahashi, Tsuyoshi, Yokoyama, Yuhei, Bery, Amit I., Mineura, Katsutaka, Bai, Yun Zhu, Ritter, Jon H., Hachem, Ramsey R., Bharat, Ankit, Lavine, Kory J., Nava, Ruben G., Puri, Varun, Krupnick, Alexander S., Gelman, Andrew E., Reed, Hasina Outtz, Wong, Brian W., and Kreisel, Daniel

Published
2024
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14. Ex vivo lung perfusion in donation after circulatory death: A post hoc analysis of the Normothermic Ex Vivo Lung Perfusion as an Assessment of Extended/Marginal Donors Lungs trial

Author

Sanchez, Pablo G., Ryan, John P., Davis, Robert D., Hartwig, Matthew G., Machuca, Tiago N., Daneshmand, Mani A., D’Ovidio, Frank, D’Cunha, Jonathan, Bermudez, Christian A., Weyant, Michael J., Jessen, Michael E., Mulligan, Michael S., Wozniak, Thomas, Lynch, William, Nemeh, Hassan, Caldeira, Christiano, Song, Tae, Kreisel, Daniel, Camp, Phillip C., Ramzy, Danny, Griffith, Bartley P., Cantu, Edward, Whitson, Bryan A., Gouchoe, Doug A., Wozniak, Thomas C., Kon, Zachary N., and Lynch, William R.

Published
2024
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17. Defining a natural killer cell-enriched molecular rejection-like state in lung transplant transbronchial biopsies

Author

Gauthier, Patrick T., Mackova, Martina, Hirji, Alim, Weinkauf, Justin, Timofte, Irina L., Snell, Greg I., Westall, Glen P., Havlin, Jan, Lischke, Robert, Zajacová, Andrea, Simonek, Jan, Hachem, Ramsey, Kreisel, Daniel, Levine, Deborah, Kubisa, Bartosz, Piotrowska, Maria, Juvet, Stephen, Keshavjee, Shaf, Jaksch, Peter, Klepetko, Walter, Halloran, Kieran, and Halloran, Philip F.

Published
2023
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37. Transcripts associated with chronic lung allograft dysfunction in transbronchial biopsies of lung transplants

Author

Parkes, Michael D., Halloran, Kieran, Hirji, Alim, Pon, Shane, Weinkauf, Justin, Timofte, Irina L., Snell, Greg I., Westall, Glen P., Havlin, Jan, Lischke, Robert, Zajacová, Andrea, Hachem, Ramsey, Kreisel, Daniel, Levine, Deborah, Kubisa, Bartosz, Piotrowska, Maria, Juvet, Stephen, Keshavjee, Shaf, Jaksch, Peter, Klepetko, Walter, and Halloran, Philip F.

Published
2022
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39. Stress-induced eosinophil activation contributes to postoperative morbidity and mortality after lung resection.

Author

Mei, Zhongcheng, Khalil, May A., Guo, Yizhan, Li, Dongge, Banerjee, Anirban, Taheri, Mojtaba, Kratzmeier, Christina M., Chen, Kelly, Lau, Christine L., Luzina, Irina G., Atamas, Sergei P., Kandasamy, Sivaveera, Kreisel, Daniel, Gelman, Andrew E., Jacobsen, Elizabeth A., and Krupnick, Alexander Sasha

Subjects
GRANULOCYTE-macrophage colony-stimulating factor, NITRIC-oxide synthases, INNATE lymphoid cells, ABDOMINAL surgery, LUNG surgery, PNEUMONECTOMY
Abstract

Respiratory failure occurs more frequently after thoracic surgery than abdominal surgery. Although the etiology for this complication is frequently attributed to underlying lung disease present in patients undergoing thoracic surgery, this notion is often unfounded because many patients with normal preoperative pulmonary function often require prolonged oxygen supplementation even after minimal resection of lung tissue. Using a murine model of pulmonary resection and peripheral blood samples from patients undergoing resection of the lung or abdominal organs, we demonstrated that lung surgery initiates a proinflammatory loop that results in damage to the remaining lung tissue, noncardiogenic pulmonary edema, hypoxia, and even death. Specifically, we demonstrated that resection of murine lung tissue increased concentrations of the homeostatic cytokine interleukin-7, which led to local and systemic activation of type 2 innate lymphoid cells. This process activated lung-resident eosinophils and facilitated stress-induced eosinophil maturation in the bone marrow in a granulocyte-macrophage colony-stimulating factor–dependent manner, resulting in systemic eosinophilia in both mice and humans. Up-regulation of inducible nitric oxide synthase in lung-resident eosinophils led to tissue nitrosylation, pulmonary edema, hypoxia, and, at times, death. Disrupting this activation cascade at any stage ameliorated deleterious outcomes and improved survival after lung resection in the mouse model. Our data suggest that repurposing US Food and Drug Administration–approved eosinophil-targeting strategies may potentially offer a therapeutic intervention to improve outcomes for patients who require lung resection for benign or malignant etiology. Editor's summary: Respiratory failure frequently occurs after lung resection and may not be fully explained by underlying respiratory disease or the size of the resection. Here, Mei and colleagues used patient samples and mouse models of pneumonectomy to show that lung resection specifically leads to increased percentages of eosinophils through a mechanism involving production of IL-7 by γδ T cells, leading to granulocyte-macrophage colony-stimulating factor production by type 2 innate lymphoid cells, ultimately resulting in increased eosinophil maturation, activation, and production of reactive oxygen species that injure the remaining lung. Targeting different points in this pathway reduced lung damage and improved survival of mice after lung resection, suggesting that perioperative administration of agents that target eosinophils or neutralize nitric oxide synthase could potentially reduce the risk of respiratory failure after lung resection. —Melissa L. Norton [ABSTRACT FROM AUTHOR]

Published
2024
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41. Ex Vivo Lung Perfusion in Donation after Circulatory Death: A Post-Hoc Analysis of the NOVEL Trial

Author

Gouchoe, Doug A., primary, Sanchez, Pablo G., additional, D’Cunha, Jonathan, additional, Bermudez, Christian A., additional, Daneshmand, Mani A., additional, Davis, Robert D., additional, Hartwig, Matthew G., additional, Wozniak, Thomas C., additional, Kon, Zachary N., additional, Griffith, Bartley P., additional, Lynch, William R., additional, Machuca, Tiago N., additional, Weyant, Michael J., additional, Jessen, Michael E., additional, Mulligan, Michael S., additional, D’Ovidio, Frank, additional, Camp, Phillip C., additional, Cantu, Edward, additional, Whitson, Bryan A., additional, Ryan, John P., additional, Wozniak, Thomas, additional, Lynch, William, additional, Nemeh, Hassan, additional, Caldeira, Christiano, additional, Song, Tae, additional, Kreisel, Daniel, additional, and Ramzy, Danny, additional

Published
2024
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45. Impact of Nighttime Lung Transplantation on Outcomes and Costs

Author

Yang, Zhizhou, Takahashi, Tsuyoshi, Gerull, William D., Hamilton, Christy, Subramanian, Melanie P., Liu, Jingxia, Meyers, Bryan F., Kozower, Benjamin D., Patterson, G. Alexander, Nava, Ruben G., Hachem, Ramsey R., Witt, Chad A., Aguilar, Patrick R., Pasque, Michael K., Byers, Derek E., Kulkarni, Hrishikesh S., Kreisel, Daniel, and Puri, Varun

Published
2021
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47. Models of Lung Transplant Research: a consensus statement from the National Heart, Lung, and Blood Institute workshop

Author

Lama, Vibha N, Belperio, John A, Christie, Jason D, El-Chemaly, Souheil, Fishbein, Michael C, Gelman, Andrew E, Hancock, Wayne W, Keshavjee, Shaf, Kreisel, Daniel, Laubach, Victor E, Looney, Mark R, McDyer, John F, Mohanakumar, Thalachallour, Shilling, Rebecca A, Panoskaltsis-Mortari, Angela, Wilkes, David S, Eu, Jerry P, and Nicolls, Mark R

Subjects
Lung, Rare Diseases, Acute Respiratory Distress Syndrome, Organ Transplantation, Transplantation, Respiratory, Immunology
Abstract

Lung transplantation, a cure for a number of end-stage lung diseases, continues to have the worst long-term outcomes when compared with other solid organ transplants. Preclinical modeling of the most common and serious lung transplantation complications are essential to better understand and mitigate the pathophysiological processes that lead to these complications. Various animal and in vitro models of lung transplant complications now exist and each of these models has unique strengths. However, significant issues, such as the required technical expertise as well as the robustness and clinical usefulness of these models, remain to be overcome or clarified. The National Heart, Lung, and Blood Institute (NHLBI) convened a workshop in March 2016 to review the state of preclinical science addressing the three most important complications of lung transplantation: primary graft dysfunction (PGD), acute rejection (AR), and chronic lung allograft dysfunction (CLAD). In addition, the participants of the workshop were tasked to make consensus recommendations on the best use of these complimentary models to close our knowledge gaps in PGD, AR, and CLAD. Their reviews and recommendations are summarized in this report. Furthermore, the participants outlined opportunities to collaborate and directions to accelerate research using these preclinical models.

Published
2017

48. IL-1[beta]-dependent extravasation of preexisting lung-restricted autoantibodies during lung transplantation activates complement and mediates primary graft dysfunction

Author

Yang, Wenbin, Cerier, Emily Jeong, Nunez-Santana, Felix L., Wu, Qiang, Yan, Yuanqing, Kurihara, Chitaru, Liu, Xianpeng, Yeldandi, Anjana, Khurram, Nigar, Avella-Patino, Diego, Sun, Haiying, Budinger, G.R. Scott, Kreisel, Daniel, Mohanakumar, Thalachallour, Lecuona, Emilia, and Bharat, Ankit

Subjects
Lungs -- Transplantation, Autoantibodies -- Physiological aspects -- Health aspects, Graft rejection -- Risk factors, Interleukin-1 -- Physiological aspects -- Health aspects, Health care industry
Abstract

Preexisting lung-restricted autoantibodies (LRAs) are associated with a higher incidence of primary graft dysfunction (PGD), although it remains unclear whether LRAs can drive its pathogenesis. In syngeneic murine left lung transplant recipients, preexisting LRAs worsened graft dysfunction, which was evident by impaired gas exchange, increased pulmonary edema, and activation of damage-associated pathways in lung epithelial cells. LRA-mediated injury was distinct from ischemia-reperfusion injury since deletion of donor nonclassical monocytes and host neutrophils could not prevent graft dysfunction in LRA-pretreated recipients. Whole LRA IgG molecules were necessary for lung injury, which was mediated by the classical and alternative complement pathways and reversed by complement inhibition. However, deletion of Fc receptors in donor macrophages or mannose-binding lectin in recipient mice failed to rescue lung function. LRA-mediated injury was localized to the transplanted lung and dependent on IL-1[beta]-mediated permeabilization of pulmonary vascular endothelium, which allowed extravasation of antibodies. Genetic deletion or pharmacological inhibition of IL-1R in the donor lungs prevented LRA-induced graft injury. In humans, preexisting LRAs were an independent risk factor for severe PGD and could be treated with plasmapheresis and complement blockade. We conclude that preexisting LRAs can compound ischemia-reperfusion injury to worsen PGD for which complement inhibition may be effective., Introduction Primary graft dysfunction (PGD) affects over 50% of recipients following lung transplantation and has emerged as the principal risk factor for both short-term mortality as well as long-term graft [...]

Published
2022
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49. Reprogramming alveolar macrophage responses to TGF-[beta]] reveals [CCR2.sup.+] monocyte activity that promotes bronchiolitis obliterans syndrome

Author

Liu, Zhiyi, Liao, Fuyi, Zhu, Jihong, Zhou, Dequan, Heo, Gyu Seong, Leuhmann, Hannah P., Scozzi, Davide, Parks, Antanisha, Hachem, Ramsey, Byers, Derek E., Tague, Laneshia K., Kulkarni, Hrishikesh S., Cano, Marlene, Wong, Brian W., Li, Wenjun, Haung, Howard J., Krupnick, Alexander S., Kreisel, Daniel, Liu, Yongjian, and Gelman, Andrew E.

Subjects
Transplantation of organs, tissues, etc. -- Patient outcomes, Bronchiolitis -- Diagnosis -- Care and treatment, Immunotherapy -- Patient outcomes, Macrophages -- Analysis, Transforming growth factors -- Analysis, Health care industry
Abstract

Bronchiolitis obliterans syndrome (BOS) is a major impediment to lung transplant survival and is generally resistant to medical therapy. Extracorporeal photophoresis (ECP) is an immunomodulatory therapy that shows promise in stabilizing BOS patients, but its mechanisms of action are unclear. In a mouse lung transplant model, we show that ECP blunts alloimmune responses and inhibits BOS through lowering airway TGF-[beta] bioavailability without altering its expression. Surprisingly, ECP-treated leukocytes were primarily engulfed by alveolar macrophages (AMs), which were reprogrammed to become less responsive to TGF-[beta] and reduce TGF-[beta] bioavailability through secretion of the TGF-[beta] antagonist decorin. In untreated recipients, high airway TGF-[beta] activity stimulated AMs to express CCL2, leading to [CCR2.sup.+] monocyte-driven BOS development. Moreover, we found TGF-[beta] receptor 2-dependent differentiation of [CCR2.sup.+] monocytes was required for the generation of monocyte-derived AMs, which in turn promoted BOS by expanding tissue-resident memory CD8* T cells that inflicted airway injury through Blimp-1-mediated granzyme B expression. Thus, through studying the effects of ECP, we have identified an AM functional plasticity that controls a TGF-[beta]-dependent network that couples [CCR2.sup.+] monocyte recruitment and differentiation to alloimmunity and BOS., Introduction Bronchiolitis obliterans syndrome (BOS) is the most common form of chronic lung allograft dysfunction (CLAD) and the leading cause of rejection after the first year of transplantation (1). The [...]

Published
2022
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50. Molecular T-cell‒mediated rejection in transbronchial and mucosal lung transplant biopsies is associated with future risk of graft loss

Author

Halloran, Kieran, Parkes, Michael D., Timofte, Irina, Snell, Gregory, Westall, Glen, Havlin, Jan, Lischke, Robert, Hachem, Ramsey, Kreisel, Daniel, Levine, Deborah, Kubisa, Bartosz, Piotrowska, Maria, Juvet, Stephen, Keshavjee, Shaf, Jaksch, Peter, Klepetko, Walter, Hirji, Alim, Weinkauf, Justin, and Halloran, Philip F.

Published
2020
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