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Your search keyword '"Hasan H. Öz"' showing total 3 results
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3 results on '"Hasan H. Öz"'

1. Pathogenic fungi regulate immunity by inducing neutrophilic myeloid-derived suppressor cells.

Author

Rieber N, Singh A, Öz H, Carevic M, Bouzani M, Amich J, Ost M, Ye Z, Ballbach M, Schäfer I, Mezger M, Klimosch SN, Weber AN, Handgretinger R, Krappmann S, Liese J, Engeholm M, Schüle R, Salih HR, Marodi L, Speckmann C, Grimbacher B, Ruland J, Brown GD, Beilhack A, Loeffler J, and Hartl D

Subjects
Animals, Aspergillosis immunology, Aspergillosis microbiology, CARD Signaling Adaptor Proteins metabolism, Candidiasis immunology, Candidiasis microbiology, Cells, Cultured, Disease Models, Animal, Humans, Lectins, C-Type metabolism, Mice, Signal Transduction, Aspergillus fumigatus immunology, Candida albicans immunology, Host-Pathogen Interactions, Immune Tolerance, Neutrophils immunology
Abstract

Despite continuous contact with fungi, immunocompetent individuals rarely develop pro-inflammatory antifungal immune responses. The underlying tolerogenic mechanisms are incompletely understood. Using both mouse models and human patients, we show that infection with the human pathogenic fungi Aspergillus fumigatus and Candida albicans induces a distinct subset of neutrophilic myeloid-derived suppressor cells (MDSCs), which functionally suppress T and NK cell responses. Mechanistically, pathogenic fungi induce neutrophilic MDSCs through the pattern recognition receptor Dectin-1 and its downstream adaptor protein CARD9. Fungal MDSC induction is further dependent on pathways downstream of Dectin-1 signaling, notably reactive oxygen species (ROS) generation as well as caspase-8 activity and interleukin-1 (IL-1) production. Additionally, exogenous IL-1β induces MDSCs to comparable levels observed during C. albicans infection. Adoptive transfer and survival experiments show that MDSCs are protective during invasive C. albicans infection, but not A. fumigatus infection. These studies define an innate immune mechanism by which pathogenic fungi regulate host defense., (Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.)

Published
2015
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2. Human neutrophil development and functionality are enabled in a humanized mouse model

Author

Yunjiang Zheng, Esen Sefik, John Astle, Kutay Karatepe, Hasan H. Öz, Angel G. Solis, Ruaidhrí Jackson, Hongbo R. Luo, Emanuela M. Bruscia, Stephanie Halene, Liang Shan, and Richard A. Flavell

Subjects
Mice, Multidisciplinary, Neutrophils, Receptors, Granulocyte Colony-Stimulating Factor, Granulocyte Colony-Stimulating Factor, Humans, Animals, Granulocyte-Macrophage Colony-Stimulating Factor, Cytokines
Abstract

Mice with a functional human immune system serve as an invaluable tool to study the development and function of the human immune system in vivo. A major technological limitation of all current humanized mouse models is the lack of mature and functional human neutrophils in circulation and tissues. To overcome this, we generated a humanized mouse model named MISTRGGR, in which the mouse granulocyte colony-stimulating factor (G-CSF) was replaced with human G-CSF and the mouse G-CSF receptor gene was deleted in existing MISTRG mice. By targeting the G-CSF cytokine-receptor axis, we dramatically improved the reconstitution of mature circulating and tissue-infiltrating human neutrophils in MISTRGGR mice. Moreover, these functional human neutrophils in MISTRGGR are recruited upon inflammatory and infectious challenges and help reduce bacterial burden. MISTRGGR mice represent a unique mouse model that finally permits the study of human neutrophils in health and disease.

Published
2022

3. Recruited monocytes/macrophages drive pulmonary neutrophilic inflammation and irreversible lung tissue remodeling in cystic fibrosis

Author

Hasan H. Öz, Ee-Chun Cheng, Caterina Di Pietro, Toma Tebaldi, Giulia Biancon, Caroline Zeiss, Ping-Xia Zhang, Pamela H. Huang, Sofia S. Esquibies, Clemente J. Britto, Jonas C. Schupp, Thomas S. Murray, Stephanie Halene, Diane S. Krause, Marie E. Egan, and Emanuela M. Bruscia

Subjects
History, Cystic Fibrosis, Polymers and Plastics, RNA biology, Cystic Fibrosis Transmembrane Conductance Regulator, lung remodeling, Monocytes, Industrial and Manufacturing Engineering, General Biochemistry, Genetics and Molecular Biology, cystic fibrosis, Mice, computational biology, neutrophils, Transforming Growth Factor beta, Immunology, c-c motif chemokine receptor 2, chronic lung inflammation, lipopolysaccharide, macrophages, monocytes, recruitment, transforming growth factor β, RNA-seq, single cell RNA-seq, omics, sequencing, network analysis [CP], Humans, Animals, Business and International Management, Lung, network analysis, Inflammation, Macrophages, Pneumonia, Immunology [CP], Receptors, Chemokine
Abstract

Persistent neutrophil-dominated lung inflammation contributes to lung damage in cystic fibrosis (CF). However, the mechanisms that drive persistent lung neutrophilia and tissue deterioration in CF are not well characterized. Starting from the observation that, in patients with CF, c-c motif chemokine receptor 2 (CCR2)

Published
2022
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