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15 results on '"Buang, Norzawani"'

1. Multi-omics identify falling LRRC15 as a COVID-19 severity marker and persistent pro-thrombotic signals in convalescence

Author

Gisby, Jack S., Buang, Norzawani B., Papadaki, Artemis, Clarke, Candice L., Malik, Talat H., Medjeral-Thomas, Nicholas, Pinheiro, Damiola, Mortimer, Paige M., Lewis, Shanice, Sandhu, Eleanor, McAdoo, Stephen P., Prendecki, Maria F., Willicombe, Michelle, Pickering, Matthew C., Botto, Marina, Thomas, David C., and Peters, James E.

Published
2022
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2. Genetic and cellular mechanisms of autoimmunity in lupus-prone B6.129-Sle16 mice

Author

Buang, Norzawani Binti, Botto, Marina, and Carlucci, Francesco

Subjects
610
Abstract

Genome sequencing and transcriptomic analyses are hypothesis-free approaches to identify genetic variants(s) and biological pathway(s) associated with a disease. T cells are paramount in the pathogenesis of systemic lupus erythematosus (SLE). Hyperactive CD4+ T cells can promote the production of auto-antibodies by offering excessive help to B cells. B6 congenic mice carrying the Sle16 locus (B6.129-Sle16) have increased auto-antibody levels, mild glomerulonephritis, and hyperactive T and B cells. These data indicate that intrinsic T cell abnormalities might drive the lupus-like disease development in B6.129-Sle16 mice. The aim of my thesis was to use exome sequencing and transcriptomic analysis of B6.129-Sle16 T cells from pre-disease mice to identify new candidate gene(s) and pathway(s) in lupus. Exome sequencing analysis uncovered 35 candidate genes with functional variants. RNAseq analysis of CD4+ and CD8+ T cells showed that the PYHIN gene family (Pydc4, Pydc3, Pyhin1 and Ifi204 genes) was the most differentially expressed in B6.129-Sle16 mice compared to B6 controls. PYHIN gene family expression is induced by type I interferon (IFN) and an increased IFN signature is a well-known characteristic in SLE. In my study, using in-vitro, in-vivo and ex-vivo analyses, I found no differences in the expression of IFN-inducible genes nor in pDC activation between B6.129-Sle16 mice and B6 controls. However, I observed that Pydc4 and Ifi204 gene expression could be modulated via anti-CD3 stimulation, indicating that these genes might directly regulate T cell proliferation, independent of type I IFN signalling. Altogether my findings identified new genes relevant to SLE and showed that the lupus-like disease in B6.129-Sle16 mice is independent of type I IFN, supporting the notion that lupus pathogenesis is driven by several mechanisms.

Published
2017
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5. Multi-omics identify LRRC15 as a COVID-19 severity predictor and persistent pro-thrombotic signals in convalescence

Author

Gisby, Jack S., primary, Buang, Norzawani B., additional, Papadaki, Artemis, additional, Clarke, Candice L., additional, Malik, Talat H., additional, Medjeral-Thomas, Nicholas, additional, Pinheiro, Damiola, additional, Mortimer, Paige M., additional, Lewis, Shanice, additional, Sandhu, Eleanor, additional, McAdoo, Stephen P., additional, Prendecki, Maria F., additional, Willicombe, Michelle, additional, Pickering, Matthew C., additional, Botto, Marina, additional, Thomas, David C., additional, and Peters, James E., additional

Published
2022
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6. Longitudinal proteomic profiling of dialysis patients with COVID-19 reveals markers of severity and predictors of death

Author

Gisby, Jack, primary, Clarke, Candice L, additional, Medjeral-Thomas, Nicholas, additional, Malik, Talat H, additional, Papadaki, Artemis, additional, Mortimer, Paige M, additional, Buang, Norzawani B, additional, Lewis, Shanice, additional, Pereira, Marie, additional, Toulza, Frederic, additional, Fagnano, Ester, additional, Mawhin, Marie-Anne, additional, Dutton, Emma E, additional, Tapeng, Lunnathaya, additional, Richard, Arianne C, additional, Kirk, Paul DW, additional, Behmoaras, Jacques, additional, Sandhu, Eleanor, additional, McAdoo, Stephen P, additional, Prendecki, Maria F, additional, Pickering, Matthew C, additional, Botto, Marina, additional, Willicombe, Michelle, additional, Thomas, David C, additional, and Peters, James E, additional

Published
2021
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7. Author response: Longitudinal proteomic profiling of dialysis patients with COVID-19 reveals markers of severity and predictors of death

Author

Gisby, Jack, primary, Clarke, Candice L, additional, Medjeral-Thomas, Nicholas, additional, Malik, Talat H, additional, Papadaki, Artemis, additional, Mortimer, Paige M, additional, Buang, Norzawani B, additional, Lewis, Shanice, additional, Pereira, Marie, additional, Toulza, Frederic, additional, Fagnano, Ester, additional, Mawhin, Marie-Anne, additional, Dutton, Emma E, additional, Tapeng, Lunnathaya, additional, Richard, Arianne C, additional, Kirk, Paul DW, additional, Behmoaras, Jacques, additional, Sandhu, Eleanor, additional, McAdoo, Stephen P, additional, Prendecki, Maria F, additional, Pickering, Matthew C, additional, Botto, Marina, additional, Willicombe, Michelle, additional, Thomas, David C, additional, and Peters, James E, additional

Published
2021
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8. Longitudinal proteomic profiling of dialysis patients with COVID-19 reveals markers of severity and predictors of death

Author

Gisby, Jack, primary, Clarke, Candice L., additional, Medjeral-Thomas, Nicholas, additional, Malik, Talat H., additional, Papadaki, Artemis, additional, Mortimer, Paige M., additional, Buang, Norzawani B., additional, Lewis, Shanice, additional, Pereira, Marie, additional, Toulza, Frederic, additional, Fagnano, Ester, additional, Mawhin, Marie-Anne, additional, Dutton, Emma E., additional, Tapeng, Lunnathaya, additional, Richard, Arianne C., additional, Kirk, Paul D. W., additional, Behmoaras, Jacques, additional, Sandhu, Eleanor, additional, McAdoo, Stephen P., additional, Prendecki, Maria F., additional, Pickering, Matthew C., additional, Botto, Marina, additional, Willicombe, Michelle, additional, Thomas, David C., additional, and Peters, James E., additional

Published
2020
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10. Acute Iron Deprivation Reprograms Human Macrophage Metabolism and Reduces Inflammation In Vivo

Author

Pereira, Marie, primary, Chen, Tai-Di, additional, Buang, Norzawani, additional, Olona, Antoni, additional, Ko, Jeong-Hun, additional, Prendecki, Maria, additional, Costa, Ana S.H., additional, Nikitopoulou, Efterpi, additional, Tronci, Laura, additional, Pusey, Charles D., additional, Cook, H. Terence, additional, McAdoo, Stephen P., additional, Frezza, Christian, additional, and Behmoaras, Jacques, additional

Published
2019
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12. BCAT1 affects mitochondrial metabolism independently of leucine transamination in activated human macrophages.

Author

Jeong-Hun Ko, Olona, Antoni, Papathanassiu, Adonia E., Buang, Norzawani, Park, Kwon-Sik, Costa, Ana S. H., Mauro, Claudio, Frezza, Christian, and Behmoaras, Jacques

Subjects
LEUCINE, MACROPHAGES, MACROPHAGE activation, METABOLISM, MITOCHONDRIA, TRICARBOXYLIC acids
Abstract

In response to environmental stimuli, macrophages change their nutrient consumption and undergo an early metabolic adaptation that progressively shapes their polarization state. During the transient, early phase of pro-inflammatory macrophage activation, an increase in tricarboxylic acid (TCA) cycle activity has been reported, but the relative contribution of branched-chain amino acid (BCAA) leucine remains to be determined. Here, we show that glucose but not glutamine is a major contributor of the increase in TCA cycle metabolites during early macrophage activation in humans.We then show that, although uptake of BCAAs is not altered, their transamination by BCAT1 is increased following 8 h lipopolysaccharide (LPS) stimulation. Of note, leucine is not metabolized to integrate into the TCA cycle in basal or stimulated human macrophages. Surprisingly, the pharmacological inhibition of BCAT1 reduced glucose-derived itaconate, α-ketoglutarate and 2-hydroxyglutarate levels without affecting succinate and citrate levels, indicating a partial inhibition of the TCA cycle. This indirect effect is associated with NRF2 (also known as NFE2L2) activation and antioxidant responses. These results suggest a moonlighting role of BCAT1 through redox-mediated control of mitochondrial function during early macrophage activation. [ABSTRACT FROM AUTHOR]

Published
2020
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14. Longitudinal proteomic profiling of dialysis patients with COVID-19 reveals markers of severity and predictors of death

Author

Gisby, Jack, Clarke, Candice L, Medjeral-Thomas, Nicholas, Malik, Talat H, Papadaki, Artemis, Mortimer, Paige M, Buang, Norzawani B, Lewis, Shanice, Pereira, Marie, Toulza, Frederic, Fagnano, Ester, Mawhin, Marie-Anne, Dutton, Emma E, Tapeng, Lunnathaya, Richard, Arianne C, Kirk, Paul Dw, Behmoaras, Jacques, Sandhu, Eleanor, McAdoo, Stephen P, Prendecki, Maria F, Pickering, Matthew C, Botto, Marina, Willicombe, Michelle, Thomas, David C, and Peters, James E

Subjects
Male, Proteomics, medicine, longitudinal, SARS-CoV-2, COVID-19, biomarkers, Middle Aged, Prognosis, Severity of Illness Index, cytokines, 3. Good health, immunology, Hospitalization, inflammation, Renal Dialysis, end-stage kidney disease, Humans, Kidney Failure, Chronic, Female, human, Longitudinal Studies, Aged, Forecasting
Abstract

End-stage kidney disease (ESKD) patients are at high risk of severe COVID-19. We measured 436 circulating proteins in serial blood samples from hospitalised and non-hospitalised ESKD patients with COVID-19 (n = 256 samples from 55 patients). Comparison to 51 non-infected patients revealed 221 differentially expressed proteins, with consistent results in a separate subcohort of 46 COVID-19 patients. Two hundred and three proteins were associated with clinical severity, including IL6, markers of monocyte recruitment (e.g. CCL2, CCL7), neutrophil activation (e.g. proteinase-3), and epithelial injury (e.g. KRT19). Machine-learning identified predictors of severity including IL18BP, CTSD, GDF15, and KRT19. Survival analysis with joint models revealed 69 predictors of death. Longitudinal modelling with linear mixed models uncovered 32 proteins displaying different temporal profiles in severe versus non-severe disease, including integrins and adhesion molecules. These data implicate epithelial damage, innate immune activation, and leucocyte-endothelial interactions in the pathology of severe COVID-19 and provide a resource for identifying drug targets.

15. Longitudinal proteomic profiling of dialysis patients with COVID-19 reveals markers of severity and predictors of death

Author

Gisby, Jack, Clarke, Candice L, Medjeral-Thomas, Nicholas, Malik, Talat H, Papadaki, Artemis, Mortimer, Paige M, Buang, Norzawani B, Lewis, Shanice, Pereira, Marie, Toulza, Frederic, Fagnano, Ester, Mawhin, Marie-Anne, Dutton, Emma E, Tapeng, Lunnathaya, Richard, Arianne C, Kirk, Paul DW, Behmoaras, Jacques, Sandhu, Eleanor, McAdoo, Stephen P, Prendecki, Maria F, Pickering, Matthew C, Botto, Marina, Willicombe, Michelle, Thomas, David C, and Peters, James E

Subjects
Immunology and Inflammation, proteomics, longitudinal, end-stage kidney disease, Medicine, COVID-19, biomarkers, cytokines, 3. Good health, Research Article, Human
Abstract

Funder: The Sidharth Burman endowment, End-stage kidney disease (ESKD) patients are at high risk of severe COVID-19. We measured 436 circulating proteins in serial blood samples from hospitalised and non-hospitalised ESKD patients with COVID-19 (n = 256 samples from 55 patients). Comparison to 51 non-infected patients revealed 221 differentially expressed proteins, with consistent results in a separate subcohort of 46 COVID-19 patients. Two hundred and three proteins were associated with clinical severity, including IL6, markers of monocyte recruitment (e.g. CCL2, CCL7), neutrophil activation (e.g. proteinase-3), and epithelial injury (e.g. KRT19). Machine-learning identified predictors of severity including IL18BP, CTSD, GDF15, and KRT19. Survival analysis with joint models revealed 69 predictors of death. Longitudinal modelling with linear mixed models uncovered 32 proteins displaying different temporal profiles in severe versus non-severe disease, including integrins and adhesion molecules. These data implicate epithelial damage, innate immune activation, and leucocyte–endothelial interactions in the pathology of severe COVID-19 and provide a resource for identifying drug targets.

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