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4 results on '"James F. George"'

1. Microanatomic Distribution of Myeloid Heme Oxygenase-1 Protects against Free Radical-Mediated Immunopathology in Human Tuberculosis

Author

Krishna C. Chinta, Md. Aejazur Rahman, Vikram Saini, Joel N. Glasgow, Vineel P. Reddy, Jeremie M. Lever, Shepherd Nhamoyebonde, Alasdair Leslie, Ryan M. Wells, Amie Traylor, Rajhmun Madansein, Gene P. Siegal, Veena B. Antony, Jessy Deshane, Gordon Wells, Kievershen Nargan, James F. George, Pratistadevi K. Ramdial, Anupam Agarwal, and Adrie J.C. Steyn

Subjects
Biology (General), QH301-705.5
Abstract

Summary: Heme oxygenase-1 (HO-1) is a cytoprotective enzyme that controls inflammatory responses and redox homeostasis; however, its role during pulmonary tuberculosis (TB) remains unclear. Using freshly resected human TB lung tissue, we examined the role of HO-1 within the cellular and pathological spectrum of TB. Flow cytometry and histopathological analysis of human TB lung tissues showed that HO-1 is expressed primarily in myeloid cells and that HO-1 levels in these cells were directly proportional to cytoprotection. HO-1 mitigates TB pathophysiology by diminishing myeloid cell-mediated oxidative damage caused by reactive oxygen and/or nitrogen intermediates, which control granulocytic karyorrhexis to generate a zonal HO-1 response. Using whole-body or myeloid-specific HO-1-deficient mice, we demonstrate that HO-1 is required to control myeloid cell infiltration and inflammation to protect against TB progression. Overall, this study reveals that zonation of HO-1 in myeloid cells modulates free-radical-mediated stress, which regulates human TB immunopathology. : Heme oxygenase-1 (HO-1) is a cytoprotective enzyme that controls inflammation and redox homeostasis; however, its role in tuberculosis (TB) is unclear. Using freshly resected human lung tissue and HO-1-deficient mice, Chinta et al. demonstrate that HO-1 in myeloid cells is important for controlling inflammatory and free-radical-mediated tissue damage in TB. Keywords: mycobacterium tuberculosis, heme oxygenase-1, human pulmonary tuberculosis, histopathological spectrum, human TB pathology, myeloid cell inflammation, macrophage, neutrophil, karyorrhexis, free radical

Published
2018
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2. Monocytes and dendritic cells in injury and regeneration

Author

Matthew D. Cheung, Elise N. Erman, Anupam Agarwal, Meryl C. Nath, and James F. George

Subjects
medicine.anatomical_structure, Myeloid, business.industry, Regeneration (biology), Cell, Immunology, medicine, Acute kidney injury, Context (language use), Mononuclear phagocyte system, medicine.disease, business, Homeostasis
Abstract

Myeloid cell populations play critical roles in the context of acute kidney injury and recovery. This chapter provides a description of acute kidney injury and an explanation of the various model systems used to study the mononuclear phagocyte system, with a focus on ischemia–reperfusion injury. The role of cellular damage caused by the initial insult and function of infiltrating versus resident cell populations through injury and recovery, or if there is a failure to restore homeostasis, are discussed.

Published
2022

3. Contributors

Author

Anupam Agarwal, Sophie L. Ashley, Amish Asthana, Anthony Atala, Janka Babickova, David P. Baird, David P. Basile, Ira Bedzow, Rohan Bhattacharya, Ulrich Blank, Joseph V. Bonventre, Nica M. Borradaile, Selin Celikoyar, Nicolas Charles, Matthew D. Cheung, Hoon Young Choi, Amanda E. Crunk, Eric Daugas, Benjamin Dekel, Marco Demaria, Danielle Diegisser, Feng Ding, Ercument Dirice, Ross Doyle, Thomas Ebert, Elise N. Erman, David A. Ferenbach, Agnes B. Fogo, Maria Giovanna Francipane, James F. George, Catherine Godson, Ladan Golestaneh, Michael S. Goligorsky, Dylan Haber, John Cijiang He, Daniel A. Heller, Jordan A. Holmes, Neil A. Hukriede, Joshua Hunsberger, Juan Carlos Izpisua Belmonte, Edgar A. Jaimes, Jing Ji, Sevim Kahraman, Titilola D. Kalejaiye, Chintan Kapadia, Matthias Kretzler, Catherine La Pointe, Laura Lasagni, Jason J. Lee, Kyung Lee, Lilach O. Lerman, Li Li, Xuezhu Li, Gretchen J. Mahler, Domenica Ida Marino, Benedetta Mazzinghi, A. Melk, Sean Muir, Samira Musah, Meryl C. Nath, Jamil Nehme, Joel Neugarten, Paola Nicolas, Mark D. Okusa, Giuseppe Orlando, Kenji Osafune, Hyeong Cheon Park, J. Geoffrey Pickering, Oren Pleniceanu, Aneta Przepiorski, May M. Rabadi, Brian B. Ratliff, Paola Romagnani, Jennifer A. Schaub, R. Schmitt, Sita Somara, Peter Stenvinkel, Marta Varela-Eirin, Ryan M. Williams, Rachel B. Wilson, Adrian S. Woolf, Yun Xia, Hai-Chun Yang, Li Yang, Mervin C. Yoder, Stephanie Zhang, Yuanyuan Zhang, and Xiang Yang Zhu

Published
2022

4. Macrophage and epithelial cell H-ferritin expression regulates renal inflammation

Author

Abolfazl Zarjou, Amie M. Traylor, Subhashini Bolisetty, James F. George, Anjana Perianayagam, Ahmed Kamal, Viktória Jeney, Anupam Agarwal, József Balla, Miguel P. Soares, Paolo Arosio, Travis D. Hull, and Reny Joseph

Subjects
Male, Pathology, Gene Expression, Kidney, Kidney Tubules, Proximal, Mice, Fibrosis, Macrophage, Myeloid Cells, Cells, Cultured, Chemokine CCL2, Nephritis, Orvostudományok, Interleukin-10, Interleukin 10, medicine.anatomical_structure, acute kidney injury, Nephrology, medicine.symptom, Ureteral Obstruction, Macrophage colony-stimulating factor, medicine.medical_specialty, macrophage polarization, Macrophage polarization, Inflammation, Mice, Transgenic, Biology, Klinikai orvostudományok, Acute kidney injury, Ferritin, Article, Proinflammatory cytokine, medicine, Animals, RNA, Messenger, Interleukin-6, Macrophage Colony-Stimulating Factor, Macrophages, fibrosis, Epithelial Cells, Macrophage Activation, medicine.disease, Molecular biology, Mice, Inbred C57BL, Disease Models, Animal, inflammation, Apoferritins, Heme Oxygenase-1
Abstract

The deposited article is a post-print version (author's manuscript from PMC). This publication hasn't any creative commons license associated. The deposited article version contains attached the supplementary materials within the pdf. Inflammation culminating in fibrosis contributes to progressive kidney disease. Cross-talk between the tubular epithelium and interstitial cells regulates inflammation by a coordinated release of cytokines and chemokines. Here we studied the role of heme oxygenase-1 (HO-1) and the heavy subunit of ferritin (FtH) in macrophage polarization and renal inflammation. Deficiency in HO-1 was associated with increased FtH expression, accumulation of macrophages with a dysregulated polarization profile, and increased fibrosis following unilateral ureteral obstruction in mice: a model of renal inflammation and fibrosis. Macrophage polarization in vitro was predominantly dependent on FtH expression in isolated bone marrow-derived mouse monocytes. Using transgenic mice with conditional deletion of FtH in the proximal tubules (FtH(PT-/-)) or myeloid cells (FtH(LysM-/-)), we found that myeloid FtH deficiency did not affect polarization or accumulation of macrophages in the injured kidney compared with wild-type (FtH(+/+)) controls. However, tubular FtH deletion led to a marked increase in proinflammatory macrophages. Furthermore, injured kidneys from FtH(PT-/-) mice expressed significantly higher levels of inflammatory chemokines and fibrosis compared with kidneys from FtH(+/+) and FtH(LysM-/-) mice. Thus, there are differential effects of FtH in macrophages and epithelial cells, which underscore the critical role of FtH in tubular-macrophage cross-talk during kidney injury. NIH grants: (R01 DK5960, R01 DK5960, P30 DK079337, R01 DK083390); Fundação para a Ciência e Tecnologia grants: (PTDC/SAU-TOX/116627/2010, HMSP-ICT/0022/2010); European Union grant: (ERC-2011-AdG. 294709 DAMAGECONTROL); AHA grant: (11POST7600074). info:eu-repo/semantics/publishedVersion

Published
2015

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