9 results on '"Osei-Sarpong C"'
Search Results
2. Systemic alterations in neutrophils and their precursors in early-stage chronic obstructive pulmonary disease.
- Author
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Kapellos, TS, Baßler, K, Fujii, W, Nalkurthi, C, Schaar, AC, Bonaguro, L, Pecht, T, Galvao, I, Agrawal, S, Saglam, A, Dudkin, E, Frishberg, A, de Domenico, E, Horne, A, Donovan, C, Kim, RY, Gallego-Ortega, D, Gillett, TE, Ansari, M, Schulte-Schrepping, J, Offermann, N, Antignano, I, Sivri, B, Lu, W, Eapen, MS, van Uelft, M, Osei-Sarpong, C, van den Berge, M, Donker, HC, Groen, HJM, Sohal, SS, Klein, J, Schreiber, T, Feißt, A, Yildirim, AÖ, Schiller, HB, Nawijn, MC, Becker, M, Händler, K, Beyer, M, Capasso, M, Ulas, T, Hasenauer, J, Pizarro, C, Theis, FJ, Hansbro, PM, Skowasch, D, Schultze, JL, Kapellos, TS, Baßler, K, Fujii, W, Nalkurthi, C, Schaar, AC, Bonaguro, L, Pecht, T, Galvao, I, Agrawal, S, Saglam, A, Dudkin, E, Frishberg, A, de Domenico, E, Horne, A, Donovan, C, Kim, RY, Gallego-Ortega, D, Gillett, TE, Ansari, M, Schulte-Schrepping, J, Offermann, N, Antignano, I, Sivri, B, Lu, W, Eapen, MS, van Uelft, M, Osei-Sarpong, C, van den Berge, M, Donker, HC, Groen, HJM, Sohal, SS, Klein, J, Schreiber, T, Feißt, A, Yildirim, AÖ, Schiller, HB, Nawijn, MC, Becker, M, Händler, K, Beyer, M, Capasso, M, Ulas, T, Hasenauer, J, Pizarro, C, Theis, FJ, Hansbro, PM, Skowasch, D, and Schultze, JL
- Abstract
Systemic inflammation is established as part of late-stage severe lung disease, but molecular, functional, and phenotypic changes in peripheral immune cells in early disease stages remain ill defined. Chronic obstructive pulmonary disease (COPD) is a major respiratory disease characterized by small-airway inflammation, emphysema, and severe breathing difficulties. Using single-cell analyses we demonstrate that blood neutrophils are already increased in early-stage COPD, and changes in molecular and functional neutrophil states correlate with lung function decline. Assessing neutrophils and their bone marrow precursors in a murine cigarette smoke exposure model identified similar molecular changes in blood neutrophils and precursor populations that also occur in the blood and lung. Our study shows that systemic molecular alterations in neutrophils and their precursors are part of early-stage COPD, a finding to be further explored for potential therapeutic targets and biomarkers for early diagnosis and patient stratification.
- Published
- 2023
3. Apolipoprotein E controls Dectin-1-dependent development of monocyte-derived alveolar macrophages upon pulmonary β-glucan-induced inflammatory adaptation
- Author
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Theobald, H., primary, Bejarano, D.A., additional, Katzmarski, N., additional, Haub, J., additional, Schulte-Schrepping, J., additional, Yu, J., additional, Bassler, K, additional, Ćirović, B., additional, Osei-Sarpong, C., additional, Piattini, F., additional, Vornholz, L, additional, Yu, X., additional, Sheoran, S., additional, Al Jawazneh, A., additional, Chakarov, S., additional, Haendler, K, additional, Brown, G.D., additional, Williams, D.L., additional, Bosurgi, L., additional, Ginhoux, F., additional, Ruland, J., additional, Beyer, M., additional, Greter, M., additional, Kopf, M., additional, Schultze, J.L., additional, and Schlitzer, A., additional
- Published
- 2022
- Full Text
- View/download PDF
4. Effect of Xylopic Acid on Paclitaxel-induced Neuropathic pain in rats
- Author
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Ameyaw, EO, primary, Boampong, JN, additional, Kukuia, KE, additional, Amoateng, P, additional, Obese, E, additional, Osei-Sarpong, C, additional, and Woode, E, additional
- Published
- 2014
- Full Text
- View/download PDF
5. Regional desynchronization of microglial activity is associated with cognitive decline in Alzheimer's disease.
- Author
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Zatcepin A, Gnörich J, Rauchmann BS, Bartos LM, Wagner S, Franzmeier N, Malpetti M, Xiang X, Shi Y, Parhizkar S, Grosch M, Wind-Mark K, Kunte ST, Beyer L, Meyer C, Brösamle D, Wendeln AC, Osei-Sarpong C, Heindl S, Liesz A, Stoecklein S, Biechele G, Finze A, Eckenweber F, Lindner S, Rominger A, Bartenstein P, Willem M, Tahirovic S, Herms J, Buerger K, Simons M, Haass C, Rupprecht R, Riemenschneider MJ, Albert NL, Beyer M, Neher JJ, Paeger L, Levin J, Höglinger GU, Perneczky R, Ziegler SI, and Brendel M
- Subjects
- Animals, Mice, Humans, Disease Models, Animal, Positron-Emission Tomography, Receptors, GABA metabolism, Male, Mice, Transgenic, Connectome methods, Female, Microglia metabolism, Alzheimer Disease metabolism, Alzheimer Disease pathology, Cognitive Dysfunction metabolism, Brain metabolism, Brain pathology
- Abstract
Background: Microglial activation is one hallmark of Alzheimer disease (AD) neuropathology but the impact of the regional interplay of microglia cells in the brain is poorly understood. We hypothesized that microglial activation is regionally synchronized in the healthy brain but experiences regional desynchronization with ongoing neurodegenerative disease. We addressed the existence of a microglia connectome and investigated microglial desynchronization as an AD biomarker., Methods: To validate the concept, we performed microglia depletion in mice to test whether interregional correlation coefficients (ICCs) of 18 kDa translocator protein (TSPO)-PET change when microglia are cleared. Next, we evaluated the influence of dysfunctional microglia and AD pathophysiology on TSPO-PET ICCs in the mouse brain, followed by translation to a human AD-continuum dataset. We correlated a personalized microglia desynchronization index with cognitive performance. Finally, we performed single-cell radiotracing (scRadiotracing) in mice to ensure the microglial source of the measured desynchronization., Results: Microglia-depleted mice showed a strong ICC reduction in all brain compartments, indicating microglia-specific desynchronization. AD mouse models demonstrated significant reductions of microglial synchronicity, associated with increasing variability of cellular radiotracer uptake in pathologically altered brain regions. Humans within the AD-continuum indicated a stage-depended reduction of microglia synchronicity associated with cognitive decline. scRadiotracing in mice showed that the increased TSPO signal was attributed to microglia., Conclusion: Using TSPO-PET imaging of mice with depleted microglia and scRadiotracing in an amyloid model, we provide first evidence that a microglia connectome can be assessed in the mouse brain. Microglia synchronicity is closely associated with cognitive decline in AD and could serve as an independent personalized biomarker for disease progression., (© 2024. The Author(s).)
- Published
- 2024
- Full Text
- View/download PDF
6. Fetal liver macrophages contribute to the hematopoietic stem cell niche by controlling granulopoiesis.
- Author
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Kayvanjoo AH, Splichalova I, Bejarano DA, Huang H, Mauel K, Makdissi N, Heider D, Tew HM, Balzer NR, Greto E, Osei-Sarpong C, Baßler K, Schultze JL, Uderhardt S, Kiermaier E, Beyer M, Schlitzer A, and Mass E
- Subjects
- Animals, Mice, Hematopoietic Stem Cells, Cell Differentiation, Erythropoiesis, Liver, Stem Cell Niche genetics, Hematopoiesis genetics, Macrophages
- Abstract
During embryogenesis, the fetal liver becomes the main hematopoietic organ, where stem and progenitor cells as well as immature and mature immune cells form an intricate cellular network. Hematopoietic stem cells (HSCs) reside in a specialized niche, which is essential for their proliferation and differentiation. However, the cellular and molecular determinants contributing to this fetal HSC niche remain largely unknown. Macrophages are the first differentiated hematopoietic cells found in the developing liver, where they are important for fetal erythropoiesis by promoting erythrocyte maturation and phagocytosing expelled nuclei. Yet, whether macrophages play a role in fetal hematopoiesis beyond serving as a niche for maturing erythroblasts remains elusive. Here, we investigate the heterogeneity of macrophage populations in the murine fetal liver to define their specific roles during hematopoiesis. Using a single-cell omics approach combined with spatial proteomics and genetic fate-mapping models, we found that fetal liver macrophages cluster into distinct yolk sac-derived subpopulations and that long-term HSCs are interacting preferentially with one of the macrophage subpopulations. Fetal livers lacking macrophages show a delay in erythropoiesis and have an increased number of granulocytes, which can be attributed to transcriptional reprogramming and altered differentiation potential of long-term HSCs. Together, our data provide a detailed map of fetal liver macrophage subpopulations and implicate macrophages as part of the fetal HSC niche., Competing Interests: AK, IS, DB, HH, KM, NM, DH, HT, NB, EG, CO, KB, JS, SU, EK, MB, AS, EM No competing interests declared, (© 2024, Kayvanjoo et al.)
- Published
- 2024
- Full Text
- View/download PDF
7. Systemic alterations in neutrophils and their precursors in early-stage chronic obstructive pulmonary disease.
- Author
-
Kapellos TS, Baßler K, Fujii W, Nalkurthi C, Schaar AC, Bonaguro L, Pecht T, Galvao I, Agrawal S, Saglam A, Dudkin E, Frishberg A, de Domenico E, Horne A, Donovan C, Kim RY, Gallego-Ortega D, Gillett TE, Ansari M, Schulte-Schrepping J, Offermann N, Antignano I, Sivri B, Lu W, Eapen MS, van Uelft M, Osei-Sarpong C, van den Berge M, Donker HC, Groen HJM, Sohal SS, Klein J, Schreiber T, Feißt A, Yildirim AÖ, Schiller HB, Nawijn MC, Becker M, Händler K, Beyer M, Capasso M, Ulas T, Hasenauer J, Pizarro C, Theis FJ, Hansbro PM, Skowasch D, and Schultze JL
- Subjects
- Humans, Animals, Mice, Neutrophils, Lung, Inflammation, Pulmonary Disease, Chronic Obstructive drug therapy, Pulmonary Emphysema
- Abstract
Systemic inflammation is established as part of late-stage severe lung disease, but molecular, functional, and phenotypic changes in peripheral immune cells in early disease stages remain ill defined. Chronic obstructive pulmonary disease (COPD) is a major respiratory disease characterized by small-airway inflammation, emphysema, and severe breathing difficulties. Using single-cell analyses we demonstrate that blood neutrophils are already increased in early-stage COPD, and changes in molecular and functional neutrophil states correlate with lung function decline. Assessing neutrophils and their bone marrow precursors in a murine cigarette smoke exposure model identified similar molecular changes in blood neutrophils and precursor populations that also occur in the blood and lung. Our study shows that systemic molecular alterations in neutrophils and their precursors are part of early-stage COPD, a finding to be further explored for potential therapeutic targets and biomarkers for early diagnosis and patient stratification., Competing Interests: Declaration of interests The authors have no competing interests., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)
- Published
- 2023
- Full Text
- View/download PDF
8. Alveolar macrophages in early stage COPD show functional deviations with properties of impaired immune activation.
- Author
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Baßler K, Fujii W, Kapellos TS, Dudkin E, Reusch N, Horne A, Reiz B, Luecken MD, Osei-Sarpong C, Warnat-Herresthal S, Bonaguro L, Schulte-Schrepping J, Wagner A, Günther P, Pizarro C, Schreiber T, Knoll R, Holsten L, Kröger C, De Domenico E, Becker M, Händler K, Wohnhaas CT, Baumgartner F, Köhler M, Theis H, Kraut M, Wadsworth MH 2nd, Hughes TK, Ferreira HJ, Hinkley E, Kaltheuner IH, Geyer M, Thiele C, Shalek AK, Feißt A, Thomas D, Dickten H, Beyer M, Baum P, Yosef N, Aschenbrenner AC, Ulas T, Hasenauer J, Theis FJ, Skowasch D, and Schultze JL
- Subjects
- Chemotaxis physiology, Humans, Macrophages metabolism, Monocytes metabolism, Macrophages, Alveolar, Pulmonary Disease, Chronic Obstructive
- Abstract
Despite its high prevalence, the cellular and molecular mechanisms of chronic obstructive pulmonary disease (COPD) are far from being understood. Here, we determine disease-related changes in cellular and molecular compositions within the alveolar space and peripheral blood of a cohort of COPD patients and controls. Myeloid cells were the largest cellular compartment in the alveolar space with invading monocytes and proliferating macrophages elevated in COPD. Modeling cell-to-cell communication, signaling pathway usage, and transcription factor binding predicts TGF-β1 to be a major upstream regulator of transcriptional changes in alveolar macrophages of COPD patients. Functionally, macrophages in COPD showed reduced antigen presentation capacity, accumulation of cholesteryl ester, reduced cellular chemotaxis, and mitochondrial dysfunction, reminiscent of impaired immune activation., Competing Interests: The handling editor [AH] declared a shared affiliation with the author(s) [AW, NY] at the time of review. BR, FB, MK and HD were employed by CommaSoft. CW and PB were employed by Boehringer Ingelheim. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be constructed as a potential conflict of interest., (Copyright © 2022 Baßler, Fujii, Kapellos, Dudkin, Reusch, Horne, Reiz, Luecken, Osei-Sarpong, Warnat-Herresthal, Bonaguro, Schulte-Schrepping, Wagner, Günther, Pizarro, Schreiber, Knoll, Holsten, Kröger, De Domenico, Becker, Händler, Wohnhaas, Baumgartner, Köhler, Theis, Kraut, Wadsworth, Hughes, Ferreira, Hinkley, Kaltheuner, Geyer, Thiele, Shalek, Feißt, Thomas, Dickten, Beyer, Baum, Yosef, Aschenbrenner, Ulas, Hasenauer, Theis, Skowasch and Schultze.)
- Published
- 2022
- Full Text
- View/download PDF
9. Enzymatic Activity of HPGD in Treg Cells Suppresses Tconv Cells to Maintain Adipose Tissue Homeostasis and Prevent Metabolic Dysfunction.
- Author
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Schmidleithner L, Thabet Y, Schönfeld E, Köhne M, Sommer D, Abdullah Z, Sadlon T, Osei-Sarpong C, Subbaramaiah K, Copperi F, Haendler K, Varga T, Schanz O, Bourry S, Bassler K, Krebs W, Peters AE, Baumgart AK, Schneeweiss M, Klee K, Schmidt SV, Nüssing S, Sander J, Ohkura N, Waha A, Sparwasser T, Wunderlich FT, Förster I, Ulas T, Weighardt H, Sakaguchi S, Pfeifer A, Blüher M, Dannenberg AJ, Ferreirós N, Muglia LJ, Wickenhauser C, Barry SC, Schultze JL, and Beyer M
- Subjects
- 3T3 Cells, Animals, Cell Line, Diabetes Mellitus, Type 2 metabolism, HEK293 Cells, Homeostasis immunology, Humans, Hydroxyprostaglandin Dehydrogenases genetics, Insulin Resistance genetics, Intra-Abdominal Fat cytology, Jurkat Cells, Lymphocyte Activation immunology, Male, Mice, Mice, Knockout, STAT5 Transcription Factor metabolism, Dinoprostone analogs & derivatives, Dinoprostone metabolism, Hydroxyprostaglandin Dehydrogenases metabolism, Intra-Abdominal Fat immunology, T-Lymphocytes, Regulatory enzymology, T-Lymphocytes, Regulatory immunology
- Abstract
Regulatory T cells (Treg cells) are important for preventing autoimmunity and maintaining tissue homeostasis, but whether Treg cells can adopt tissue- or immune-context-specific suppressive mechanisms is unclear. Here, we found that the enzyme hydroxyprostaglandin dehydrogenase (HPGD), which catabolizes prostaglandin E
2 (PGE2 ) into the metabolite 15-keto PGE2 , was highly expressed in Treg cells, particularly those in visceral adipose tissue (VAT). Nuclear receptor peroxisome proliferator-activated receptor-γ (PPARγ)-induced HPGD expression in VAT Treg cells, and consequential Treg-cell-mediated generation of 15-keto PGE2 suppressed conventional T cell activation and proliferation. Conditional deletion of Hpgd in mouse Treg cells resulted in the accumulation of functionally impaired Treg cells specifically in VAT, causing local inflammation and systemic insulin resistance. Consistent with this mechanism, humans with type 2 diabetes showed decreased HPGD expression in Treg cells. These data indicate that HPGD-mediated suppression is a tissue- and context-dependent suppressive mechanism used by Treg cells to maintain adipose tissue homeostasis., (Copyright © 2019 Elsevier Inc. All rights reserved.)- Published
- 2019
- Full Text
- View/download PDF
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