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6. Dietary lipids inhibit mitochondria transfer to macrophages to divert adipocyte-derived mitochondria into the blood

Author

Borcherding, Nicholas, Jia, Wentong, Giwa, Rocky, Field, Rachael L., Moley, John R., Kopecky, Benjamin J., Chan, Mandy M., Yang, Bin Q., Sabio, Jessica M., Walker, Emma C., Osorio, Omar, Bredemeyer, Andrea L., Pietka, Terri, Alexander-Brett, Jennifer, Morley, Sharon Celeste, Artyomov, Maxim N., Abumrad, Nada A., Schilling, Joel, Lavine, Kory, Crewe, Clair, and Brestoff, Jonathan R.

Published
2022
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7. Bronchiolitis obliterans syndrome–free survival after lung transplantation: An International Society for Heart and Lung Transplantation Thoracic Transplant Registry analysis

Author

Kulkarni, Hrishikesh S., Cherikh, Wida S., Chambers, Daniel C., Garcia, Victoria C., Hachem, Ramsey R., Kreisel, Daniel, Puri, Varun, Kozower, Benjamin D., Byers, Derek E., Witt, Chad A., Alexander-Brett, Jennifer, Aguilar, Patrick R., Tague, Laneshia K., Furuya, Yuka, Patterson, G. Alec, Trulock, Elbert P., III, and Yusen, Roger D.

Published
2019
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8. Basal epithelial stem cells cross an alarmin checkpoint for postviral lung disease

Author

Wu, Kangyun, Kamimoto, Kenji, Zhang, Yong, Yang, Kuangying, Keeler, Shamus P., Gerovac, Benjamin J., Agapov, Eugene V., Austin, Stephen P., Yantis, Jennifer, Gissy, Kelly A., Byers, Derek E., Alexander-Brett, Jennifer, Hoffmann, Christy M., Wallace, Matthew, Hughes, Michael E., Crouch, Erika C., Morris, Samantha A., and Holtzman, Michael J.

Subjects
Lung diseases -- Risk factors -- Development and progression, Immune system -- Physiological aspects -- Health aspects, Epithelial cells -- Physiological aspects -- Health aspects, Interleukins -- Physiological aspects -- Health aspects, Virus diseases -- Complications and side effects -- Physiological aspects, Health care industry
Abstract

Epithelial cells are charged with protection at barrier sites, but whether this normally beneficial response might sometimes become dysfunctional still needs definition. Here, we recognized a pattern of imbalance marked by basal epithelial cell growth and differentiation that replaced normal airspaces in a mouse model of progressive postviral lung disease due to the Sendai virus. Single-cell and lineage-tracing technologies identified a distinct subset of basal epithelial stem cells (basal ESCs) that extended into gas-exchange tissue to form long-term bronchiolar-alveolar remodeling regions. Moreover, this cell subset was selectively expanded by crossing a cell-growth and survival checkpoint linked to the nuclear-localized alarmin IL-33 that was independent of IL-33 receptor signaling and instead connected to autocrine chromatin accessibility. This mechanism creates an activated stem-progenitor cell lineage with potential for physiological or pathological function. Thus, conditional loss of Il-33 gene function in basal epithelial cells disrupted the homeostasis of the epithelial barrier at skin and gut sites but also markedly attenuated postviral disease in the lung based on the downregulation of remodeling and inflammation. Thus, we define a basal ESC strategy to deploy innate immune machinery that appears to overshoot the primordial goal of self-defense. Our findings reveal new targets to stratify and correct chronic and often deadly postviral disease., Introduction Epithelial barrier sites such as skin, gut, and lungs are charged with host protection that relies on endoderm-derived epithelial stem cells to repair any possible damage (1-3). When the [...]

Published
2021
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10. IL-33 signaling in sensory neurons promotes dry skin itch

Author

Trier, Anna M., primary, Mack, Madison R., additional, Fredman, Avery, additional, Tamari, Masato, additional, Ver Heul, Aaron M., additional, Zhao, Yonghui, additional, Guo, Changxiong J., additional, Avraham, Oshri, additional, Ford, Zachary K., additional, Oetjen, Landon K., additional, Feng, Jing, additional, Dehner, Carina, additional, Coble, Dean, additional, Badic, Asima, additional, Joshita, Satoru, additional, Kubo, Masato, additional, Gereau, Robert W., additional, Alexander-Brett, Jennifer, additional, Cavalli, Valeria, additional, Davidson, Steve, additional, Hu, Hongzhen, additional, Liu, Qin, additional, and Kim, Brian S., additional

Published
2022
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11. Age-Dependent Reduction in Asthmatic Pathology through Reprogramming of Postviral Inflammatory Responses

Author

Hazan, Guy, primary, Eubanks, Anna, additional, Gierasch, Carrie, additional, Atkinson, Jeffrey, additional, Fox, Carolyn, additional, Hernandez-Leyva, Ariel, additional, Rosen, Anne L., additional, Kau, Andrew L., additional, Agapov, Eugene, additional, Alexander-Brett, Jennifer, additional, Steinberg, Deborah, additional, Kelley, Diane, additional, White, Michael, additional, Byers, Derek, additional, Wu, Kangyun, additional, Keeler, Shamus P., additional, Zhang, Yong, additional, Koenitzer, Jeffrey R., additional, Eiden, Elise, additional, Anderson, Neil, additional, Holtzman, Michael J., additional, and Haspel, Jeffrey, additional

Published
2022
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12. Lung protective ventilation based on donor size is associated with a lower risk of severe primary graft dysfunction after lung transplantation

Author

Tague, Laneshia K., primary, Bedair, Bahaa, additional, Witt, Chad, additional, Byers, Derek E., additional, Vazquez-Guillamet, Rodrigo, additional, Kulkarni, Hrishikesh, additional, Alexander-Brett, Jennifer, additional, Nava, Ruben, additional, Puri, Varun, additional, Kreisel, Daniel, additional, Trulock, Elbert P., additional, Gelman, Andrew, additional, and Hachem, Ramsey R., additional

Published
2021
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13. Long-term IL-33-producing epithelial progenitor cells in chronic obstructive lung disease

Author

Byers, Derek E., Alexander-Brett, Jennifer, Patel, Anand C., Agapov, Eugene, Dang-Vu, Geoffrey, Jin, Xiaohua, Wu, Kangyun, You, Yingjian, Alevy, Yael, Girard, Jean-Philippe, Stappenbeck, Thaddeus S., Patterson, G. Alexander, Pierce, Richard A., Brody, Steven L., and Holtzman, Michael J.

Subjects
Lung diseases, Obstructive -- Development and progression -- Genetic aspects -- Research, Natural immunity -- Research, Interleukins -- Genetic aspects -- Physiological aspects -- Research, Epithelial cells -- Physiological aspects -- Research, Health care industry
Abstract

Chronic obstructive lung disease is characterized by persistent abnormalities in epithelial and immune cell function that are driven, at least in part, by infection. Analysis of parainfluenza virus infection in mice revealed an unexpected role for innate immune cells in IL-13-dependent chronic lung disease, but the upstream driver for the immune axis in this model and in humans with similar disease was undefined. We demonstrate here that lung levels of IL-33 are selectively increased in postviral mice with chronic obstructive lung disease and in humans with very severe chronic obstructive pulmonary disease (COPD). In the mouse model, IL-33/IL-33 receptor signaling was required for Il13 and mucin gene expression, and Il33 gene expression was localized to a virus-induced subset of airway serous cells and a constitutive subset of alveolar type 2 cells that are both linked conventionally to progenitor function. In humans with COPD, IL33 gene expression was also associated with IL13 and mucin gene expression, and IL33 induction was traceable to a subset of airway basal cells with increased capacities for pluripotency and ATP-regulated release of IL-33. Together, these findings provide a paradigm for the role of the innate immune system in chronic disease based on the influence of long-term epithelial progenitor cells programmed for excess IL-33 production., Introduction It is widely believed that the innate immune system mediates the acute response to an infectious agent, but recent work shows that this response can also translate acute infection [...]

Published
2013

14. Contributors

Author

Abadie, Valérie, primary, Abraham, Clara, additional, Adams, David H., additional, Agace, William W., additional, Alexander-Brett, Jennifer, additional, Alkhairy, Omar, additional, Ambite, Ines, additional, Anderson, Deborah J., additional, Artis, David, additional, Atmar, Robert L., additional, Aymeric, Laetitia, additional, Bachert, Claus, additional, Bakema, Jantine E., additional, Baker, Kristi, additional, Beagley, Kenneth W., additional, Befus, A.D., additional, Bemark, Mats, additional, Berin, M. Cecilia, additional, Berings, Margot, additional, Berzofsky, Jay A., additional, Bilej, Martin, additional, Biswas, Nabanita, additional, Blumberg, Richard S., additional, Bienenstock, John, additional, Bogdanos, Dimitrios, additional, Boirivant, Monica, additional, Boonnak, Kobporn, additional, Bracke, Ken R., additional, Brandtzaeg, Per, additional, Braun, Jonathan, additional, Bringer, Marie-Agnès, additional, Broadbent, Andrew J., additional, Bronson, Richard, additional, Brusselle, Guy G., additional, Bulmer, Judith N., additional, Butler, J.E., additional, Cardenas, Paul A., additional, Cebra, John J., additional, Cella, Marina, additional, Cerutti, Andrea, additional, Challacombe, Stephen J., additional, Chattha, Kuldeep, additional, Cheroutre, Hilde, additional, Chiba, Tsutomu, additional, Chorny, Alejo, additional, Clements, John D., additional, Colonna, Marco, additional, Cookson, William O.C., additional, Corbeil, Lynette B., additional, Corthésy, Blaise, additional, Cripps, Allan W., additional, van Crombruggen, Koen, additional, Pires da Cunha, Andre, additional, Cunningham-Rundles, Susanna, additional, Curtiss, Roy, additional, Darfeuille-Michaud, Arlette, additional, de Jonge, Wouter J., additional, Deban, Livija, additional, Denning, Timothy L., additional, Di Santo, James P., additional, Diefenbach, Andreas, additional, DiRita, Victor J., additional, Downey, Jordan, additional, Du, Ming-Qing, additional, Edelblum, Karen L., additional, van Egmond, Marjolein, additional, Epple, H.-J., additional, Fagarasan, Sidonia, additional, Fahey, John V., additional, Ferris, Michael J., additional, Fichtner-Feigl, Stefan, additional, Fidel, Paul L., additional, Flach, Melanie, additional, Flavell, Richard, additional, Fleit, Howard B., additional, Franchini, Genoveffa, additional, Freytag, Lucy C., additional, Fuchs, Anja, additional, Fujihashi, kohtaro, additional, Fuss, Ivan J., additional, Gagliani, Nicola, additional, Garcia, Marta Rodriguez, additional, Garrett, Wendy S., additional, Gershwin, M. Eric, additional, Gevaert, Philippe, additional, Gleeson, Maree, additional, Godaly, Gabriela, additional, Goldblum, Randall M., additional, Gour, Naina, additional, Gursel, Mayda, additional, Hajishengallis, George, additional, Hammad, Hamida, additional, Hammarström, Lennart, additional, Hänninen, Arno, additional, Hanson, Lars Å., additional, Hayday, Adrian, additional, Herzog, Ronit, additional, Hodgins, Douglas C., additional, Holgate, Stephen T., additional, Holmgren, Jan, additional, Holtzman, Michael J., additional, Hook, Edward W., additional, Huber, Samuel, additional, Hurwitz, Julia L., additional, Ivanyi, Juraj, additional, Iwasaki, Akiko, additional, Jabri, Bana, additional, Jackson, Susan, additional, Jacobs, Jonathan, additional, Jalkanen, Sirpa, additional, Janoff, Edward N., additional, Jerse, Ann E., additional, Jeyanathan, Mangalakumari, additional, Julian, Bruce A., additional, Kacskovics, Imre, additional, Kaetzel, Charlotte S., additional, Kaushic, Charu, additional, Kelsall, Brian L., additional, Kessans, Sarah, additional, Kesselring, Rebecca, additional, Kilian, Mogens, additional, Kiyono, Hiroshi, additional, Klinman, Dennis M., additional, Korotkova, Marina, additional, Kronenberg, Mitchell, additional, Krysko, Olga, additional, Kurono, Yuichi, additional, Kverka, Miloslav, additional, Lambrecht, Bart N., additional, Lamm, Michael E., additional, Lantz, Olivier, additional, Lash, Gendie E., additional, Lavelle, E.C., additional, Lefrancois, Leo, additional, Leung, Patrick S.C., additional, Levine, Myron M., additional, Lim, David J., additional, Lippolis, John, additional, Louis, Nancy A., additional, Luster, Andrew D., additional, Lutay, Nataliya, additional, Lycke, Nils, additional, Macpherson, Andrew J., additional, Mantis, Nicholas J., additional, Marcotte, Harold, additional, Martin, David H., additional, Mason, Hugh S., additional, Massa, Helen M., additional, Matoba, Nobuyuki, additional, Mayer, Lloyd, additional, Maynard, Craig L., additional, McElrath, M. Juliana, additional, McEntee, C., additional, McGhee, Jerry R., additional, McGuckin, Michael A., additional, Mestecky, Jiri, additional, Mikhak, Zamaneh, additional, Miller, Robert D., additional, Moldoveanu, Zina, additional, Montgomery, Paul C., additional, Mor, Tsafrir, additional, Neurath, Markus F., additional, Neyt, Katrijn, additional, Nicholson, Lindsay K., additional, Novak, Jan, additional, Nowicki, Stella, additional, O’Hagan, D.T., additional, O’Sullivan, Nancy L., additional, Ogra, Pearay, additional, Orihuela, Carlos, additional, Ouellette, André J., additional, Owen, Robert L., additional, Pabst, Oliver, additional, Parkos, Charles A., additional, Parreño, Viviana, additional, Patel, Mickey V., additional, Perez-Novo, Claudina, additional, Perkins, Darren J., additional, Prussin, Calman, additional, Pudney, Jeffrey, additional, Raghavan, Sukanya, additional, Rainard, Pascal, additional, Ramani, Sasirekha, additional, Randall, Troy D., additional, Raska, Milan, additional, Renukaradhya, Gourapura J., additional, Rescigno, Maria, additional, Rosenthal, Kenneth L., additional, Rothenberg, Marc E., additional, Ruemmele, Frank M., additional, Russell, Michael W., additional, Saif, Linda J., additional, Salinas, Irene, additional, Salmi, Marko, additional, Salmon, Henri, additional, Sampson, Hugh A., additional, Sansonetti, Philippe, additional, Schneider, T., additional, Serafini, Nicolas, additional, Sharma, Dolly, additional, Shen, Zheng, additional, Shi, Hai Ning, additional, Shirlaw, Penelope J., additional, Shivhare, Sourima B., additional, Smith, Phillip D., additional, Smith, Patrick M., additional, Smith, Daniel J., additional, Smythies, Lesley E., additional, Spencer, Jo, additional, Strober, Warren, additional, Subbarao, Kanta, additional, Svanborg, Catharina, additional, Svennerholm, Ann-Mari, additional, Taubman, Martin A., additional, Telemo, Esbjörn, additional, Thornhill, Martin H., additional, Thornton, David J., additional, Thuenemann, Eva, additional, Tlaskalova-Hogenova, Helena, additional, Tristram, Debra, additional, Trivedi, Palak, additional, Tuomanen, Elaine, additional, Turanek, Jaroslav, additional, Turner, Jerrold R., additional, Underdown, Brian J., additional, van Helden, Mary J., additional, Veazey, Ronald S., additional, Verdu, Elena F., additional, Vlasova, Anastasia, additional, Vliagoftis, Harissios, additional, Vogel, Stefanie N., additional, Walker, W. Allan, additional, Wang, Xiaolei, additional, Watanabe, Tomohiro, additional, Weaver, Casey T., additional, Weiner, Howard L., additional, Wells, Jerry M., additional, Wen, Ting, additional, Whittum-Hudson, Judith, additional, Whitsett, Jeffrey A., additional, Williams, Ifor R., additional, Wills-Karp, Marsha, additional, Wira, Charles R., additional, Woof, Jenny M., additional, Wotherspoon, Andrew C., additional, Xing, Zhou, additional, Xu, Huanbin, additional, Zaph, Colby, additional, Zeissig, Sebastian, additional, and Zeitz, M., additional

Published
2015
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16. Aging Regulates Post-Viral Asthmatic Airway Pathology

Author

Hazan, Guy, primary, Eubanks, Anna, additional, Gierasch, Carrie, additional, Atkinson, Jeffrey, additional, Fox, Carolyn, additional, Hernandez-Leyva, Ariel, additional, Rosen, Anne, additional, Kau, Andrew, additional, Agapov, Eugene, additional, Alexander-Brett, Jennifer, additional, Steinberg, Deborah, additional, Kelley, Diane, additional, White, Michael, additional, Byers, Derek, additional, Wu, Kangyun, additional, Keeler, Shamus, additional, Zhang, Yong, additional, Koenitzer, Jeffrey, additional, Holtzman, Michael, additional, and Haspel, Jeffrey, additional

Published
2021
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17. Epithelial IL-33 appropriates exosome trafficking for secretion in chronic airway disease

Author

Katz-Kiriakos, Ella, primary, Steinberg, Deborah F., additional, Kluender, Colin E., additional, Osorio, Omar A., additional, Newsom-Stewart, Catie, additional, Baronia, Arjun, additional, Byers, Derek E., additional, Holtzman, Michael J., additional, Katafiasz, Dawn, additional, Bailey, Kristina L., additional, Brody, Steven L., additional, Miller, Mark J., additional, and Alexander-Brett, Jennifer, additional

Published
2021
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18. Functional insights from biophysical study of TREM2 interactions with apoE and Aβ 1‐42

Author

Kober, Daniel L., primary, Stuchell‐Brereton, Melissa D., additional, Kluender, Colin E., additional, Dean, Hunter B., additional, Strickland, Michael R., additional, Steinberg, Deborah F., additional, Nelson, Samantha S., additional, Baban, Berevan, additional, Holtzman, David M., additional, Frieden, Carl, additional, Alexander‐Brett, Jennifer, additional, Roberson, Erik D., additional, Song, Yuhua, additional, and Brett, Tom J., additional

Published
2020
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19. Functional insights from biophysical study of TREM2 interactions with ApoE and Aβ1-42

Author

Kober, Daniel L., primary, Stuchell-Brereton, Melissa D., additional, Kluender, Colin E., additional, Dean, Hunter B., additional, Strickland, Michael R., additional, Steinberg, Deborah F., additional, Nelson, Samantha S., additional, Baban, Berevan, additional, Holtzman, David M., additional, Frieden, Carl, additional, Alexander-Brett, Jennifer, additional, Roberson, Erik D., additional, Song, Yuhua, additional, and Brett, Tom J., additional

Published
2020
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22. Functional insights from biophysical study of TREM2 interactions with apoE and Aβ1‐42.

Author

Kober, Daniel L., Stuchell‐Brereton, Melissa D., Kluender, Colin E., Dean, Hunter B., Strickland, Michael R., Steinberg, Deborah F., Nelson, Samantha S., Baban, Berevan, Holtzman, David M., Frieden, Carl, Alexander‐Brett, Jennifer, Roberson, Erik D., Song, Yuhua, and Brett, Tom J.

Abstract

Introduction: Triggering receptor expressed on myeloid cells‐2 (TREM2) is an immune receptor expressed on microglia that also can become soluble (sTREM2). How TREM2 engages different ligands remains poorly understood. Methods: We used comprehensive biolayer interferometry (BLI) analysis to investigate TREM2 and sTREM2 interactions with apolipoprotein E (apoE) and monomeric amyloid beta (Aβ) (mAβ42). Results: TREM2 engagement of apoE was protein mediated with little effect of lipidation, showing slight affinity differences between isoforms (E4 > E3 > E2). Another family member, TREML2, did not bind apoE. Disease‐linked TREM2 variants within a "basic patch" minimally impact apoE binding. Instead, TREM2 uses a unique hydrophobic surface to bind apoE, which requires the apoE hinge region. TREM2 and sTREM2 directly bind mAβ42 and potently inhibit Aβ42 polymerization, suggesting a potential role for soluble sTREM2 in preventing AD pathogenesis. Discussion: These findings demonstrate that TREM2 has at least two ligand‐binding surfaces that might be therapeutic targets and uncovers a potential function for sTREM2 in directly inhibiting Aβ polymerization. [ABSTRACT FROM AUTHOR]

Published
2021
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27. Defining The Importance Of Key Cytokines (TSLP, IL-25, And IL-33) Controlling IL-13 Production And Chronic Obstructive Lung Disease Under Experimental And Clinical Conditions

Author

Byers, Derek E., primary, Alexander-Brett, Jennifer, additional, Agapov, Eugene, additional, Dang-Vu, Geoffrey, additional, Jin, Xiaohua, additional, Patel, Anand C., additional, You, Yinjian, additional, Pierce, Richard A., additional, and Holtzman, Michael J., additional

Published
2012
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31. Basal epithelial stem cells cross an alarmin checkpoint for postviral lung disease.

Author

Kangyun Wu, Kenji Kamimoto, Yong Zhang, Kuangying Yang, Keeler, Shamus P., Gerovac, Benjamin J., Agapov, Eugene V., Austin, Stephen P., Yantis, Jennifer, Gissy, Kelly A., Byers, Derek E., Alexander-Brett, Jennifer, Hoffmann, Christy M., Wallace, Matthew, Hughes, Michael E., Crouch, Erika C., Morris, Samantha A., and Holtzman, Michael J.

Subjects
*RNA virus infections, *CELL differentiation, *RESEARCH, *LUNG diseases, *ANIMAL experimentation, *RESEARCH methodology, *EVALUATION research, *COMPARATIVE studies, *STEM cells, *RESEARCH funding, *PARAMYXOVIRUSES, *EPITHELIAL cells, *CYTOLOGY, *MICE, *DISEASE complications
Abstract

Epithelial cells are charged with protection at barrier sites, but whether this normally beneficial response might sometimes become dysfunctional still needs definition. Here, we recognized a pattern of imbalance marked by basal epithelial cell growth and differentiation that replaced normal airspaces in a mouse model of progressive postviral lung disease due to the Sendai virus. Single-cell and lineage-tracing technologies identified a distinct subset of basal epithelial stem cells (basal ESCs) that extended into gas-exchange tissue to form long-term bronchiolar-alveolar remodeling regions. Moreover, this cell subset was selectively expanded by crossing a cell-growth and survival checkpoint linked to the nuclear-localized alarmin IL-33 that was independent of IL-33 receptor signaling and instead connected to autocrine chromatin accessibility. This mechanism creates an activated stem-progenitor cell lineage with potential for physiological or pathological function. Thus, conditional loss of Il33 gene function in basal epithelial cells disrupted the homeostasis of the epithelial barrier at skin and gut sites but also markedly attenuated postviral disease in the lung based on the downregulation of remodeling and inflammation. Thus, we define a basal ESC strategy to deploy innate immune machinery that appears to overshoot the primordial goal of self-defense. Our findings reveal new targets to stratify and correct chronic and often deadly postviral disease. [ABSTRACT FROM AUTHOR]

Published
2021
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32. Sensory functions of motile cilia and implication for bronchiectasis.

Author

Jain R, Javidan-Nejad C, Alexander-Brett J, Horani A, Cabellon MC, Walter MJ, and Brody SL

Subjects
Animals, Humans, Kidney metabolism, Kidney pathology, Lung metabolism, Lung pathology, Polycystic Kidney, Autosomal Dominant metabolism, Polycystic Kidney, Autosomal Dominant pathology, Sensation, Signal Transduction, TRPP Cation Channels metabolism, Bronchiectasis metabolism, Bronchiectasis pathology, Cilia metabolism, Cilia pathology, Sensory Receptor Cells metabolism
Abstract

Cilia are specialized organelles that extend from the cell surface into the local environment. Cilia of the airway epithelia are motile to provide mucociliary clearance. On other cells, solitary cilia are specialized to detect chemical or mechanosensory signals. Sensory proteins in motile cilia have recently been identified that detect fluid flow, bitter taste and sex hormones. The relationship of these sensory functions in motile cilia to disease is now being revealed. An example are the polycystin-1 and polycystin-2 proteins that function as a flow sensor in kidney cilia and are mutated in autosomal dominant polycystic kidney disease (ADPKD). These polycystins are also expressed in motile cilia, potentially operating as sensors in the lung. Computed tomography studies from patients with ADPKD reveal evidence of bronchiectasis, suggesting polycystins are important in lung function. The motile cilia expression of this protein complex, as well as sensory channel TRPV4, bitter taste and sex hormones receptors, indicate that the cilia is wired to interpret environmental cues. Defective signaling of sensory proteins may result in a ciliopathy that includes lung disease.

Published
2012
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