Search

Your search keyword '"Su, Xin-zhuan"' showing total 29 results
Start Over Author "Su, Xin-zhuan" Publication Year Range Last 3 years
29 results on '"Su, Xin-zhuan"'

6. Deaggregation of mutant Plasmodium yoelii de-ubiquitinase UBP1 alters MDR1 localization to confer multidrug resistance

Author

Xu, Ruixue, primary, Lin, Lirong, additional, Jiao, Zhiwei, additional, Liang, Rui, additional, Guo, Yazhen, additional, Zhang, Yixin, additional, Shang, Xiaoxu, additional, Wang, Yuezhou, additional, Wang, Xu, additional, Yao, Luming, additional, Liu, Shengfa, additional, Deng, Xianming, additional, Yuan, Jing, additional, Su, Xin-zhuan, additional, and Li, Jian, additional

Published
2024
Full Text
View/download PDF

8. Human ApoE2 protects mice against Plasmodium berghei ANKA experimental cerebral malaria

Author

Liang, Rui, primary, Rao, Hengjun, additional, Pang, Qin, additional, Xu, Ruixue, additional, Jiao, Zhiwei, additional, Lin, Lirong, additional, Li, Li, additional, Zhong, Li, additional, Zhang, Yixin, additional, Guo, Yazhen, additional, Xiao, Nengming, additional, Liu, Shengfa, additional, Chen, Xiao-Fen, additional, Su, Xin-zhuan, additional, and Li, Jian, additional

Published
2023
Full Text
View/download PDF

9. Dysfunction of CD169 + macrophages and blockage of erythrocyte maturation as a mechanism of anemia in Plasmodium yoelii infection

Author

Tumas, Keyla C., primary, Xu, Fangzheng, additional, Wu, Jian, additional, Hernandez, Maricarmen, additional, Pattaradilokrat, Sittiporn, additional, Xia, Lu, additional, Peng, Yu-chih, additional, Lavali, Angela Musu, additional, He, Xiao, additional, Singh, Brajesh K., additional, Zhang, Cui, additional, Percopo, Caroline, additional, Qi, Chen-Feng, additional, Huang, Suming, additional, Long, Carole A., additional, and Su, Xin-zhuan, additional

Published
2023
Full Text
View/download PDF

11. Pf7: an open dataset of Plasmodium falciparum genome variation in 20,000 worldwide samples

Author

MalariaGEN, Abdel Hamid, Muzamil Mahdi, Abdelraheem, Mohamed Hassan, Acheampong, Desmond Omane, Ahouidi, Ambroise, Ali, Mozam, Almagro-Garcia, Jacob, Amambua-Ngwa, Alfred, Amaratunga, Chanaki, Amenga-Etego, Lucas, Andagalu, Ben, Anderson, Tim, Andrianaranjaka, Voahangy, Aniebo, Ifeyinwa, Aninagyei, Enoch, Ansah, Felix, Ansah, Patrick O, Apinjoh, Tobias, Arnaldo, Paulo, Ashley, Elizabeth, Auburn, Sarah, Awandare, Gordon A, Ba, Hampate, Baraka, Vito, Barry, Alyssa, Bejon, Philip, Bertin, Gwladys I, Boni, Maciej F, Borrmann, Steffen, Bousema, Teun, Bouyou-Akotet, Marielle, Branch, Oralee, Bull, Peter C, Cheah, Huch, Chindavongsa, Keobouphaphone, Chookajorn, Thanat, Chotivanich, Kesinee, Claessens, Antoine, Conway, David J, Corredor, Vladimir, Courtier, Erin, Craig, Alister, D'Alessandro, Umberto, Dama, Souleymane, Day, Nicholas, Denis, Brigitte, Dhorda, Mehul, Diakite, Mahamadou, Djimde, Abdoulaye, Dolecek, Christiane, Dondorp, Arjen, Doumbia, Seydou, Drakeley, Chris, Drury, Eleanor, Duffy, Patrick, Echeverry, Diego F, Egwang, Thomas G, Enosse, Sonia Maria Mauricio, Erko, Berhanu, Fairhurst, Rick M, Faiz, Abdul, Fanello, Caterina A, Fleharty, Mark, Forbes, Matthew, Fukuda, Mark, Gamboa, Dionicia, Ghansah, Anita, Golassa, Lemu, Goncalves, Sonia, Harrison, GL Abby, Healy, Sara Anne, Hendry, Jason A, Hernandez-Koutoucheva, Anastasia, Hien, Tran Tinh, Hill, Catherine A, Hombhanje, Francis, Hott, Amanda, Htut, Ye, Hussein, Mazza, Imwong, Mallika, Ishengoma, Deus, Jackson, Scott A, Jacob, Chris G, Jeans, Julia, Johnson, Kimberly J, Kamaliddin, Claire, Kamau, Edwin, Keatley, Jon, Kochakarn, Theerarat, Konate, Drissa S, Konaté, Abibatou, Kone, Aminatou, Kwiatkowski, Dominic P, Kyaw, Myat P, Kyle, Dennis, Lawniczak, Mara, Lee, Samuel K, Lemnge, Martha, Lim, Pharath, Lon, Chanthap, Loua, Kovana M, Mandara, Celine I, Marfurt, Jutta, Marsh, Kevin, Maude, Richard James, Mayxay, Mayfong, Maïga-Ascofaré, Oumou, Miotto, Olivo, Mita, Toshihiro, Mobegi, Victor, Mohamed, Abdelrahim Osman, Mokuolu, Olugbenga A, Montgomery, Jaqui, Morang'a, Collins Misita, Mueller, Ivo, Murie, Kathryn, Newton, Paul N, Ngo Duc, Thang, Nguyen, Thuy, Nguyen, Thuy-Nhien, Nguyen Thi Kim, Tuyen, Nguyen Van, Hong, Noedl, Harald, Nosten, Francois, Noviyanti, Rintis, Ntui, Vincent Ntui-Njock, Nzila, Alexis, Ochola-Oyier, Lynette Isabella, Ocholla, Harold, Oduro, Abraham, Omedo, Irene, Onyamboko, Marie A, Ouedraogo, Jean-Bosco, Oyebola, Kolapo, Oyibo, Wellington Aghoghovwia, Pearson, Richard, Peshu, Norbert, Phyo, Aung P, Plowe, Christopher V, Price, Ric N, Pukrittayakamee, Sasithon, Quang, Huynh Hong, Randrianarivelojosia, Milijaona, Rayner, Julian C, Ringwald, Pascal, Rosanas-Urgell, Anna, Rovira-Vallbona, Eduard, Ruano-Rubio, Valentin, Ruiz, Lastenia, Saunders, David, Shayo, Alex, Siba, Peter, Simpson, Victoria J, Sissoko, Mahamadou S, Smith, Christen, Su, Xin-Zhuan, Sutherland, Colin, Takala-Harrison, Shannon, Talman, Arthur, Tavul, Livingstone, Thanh, Ngo Viet, Thathy, Vandana, Thu, Aung Myint, Toure, Mahamoudou, Tshefu, Antoinette, Verra, Federica, Vinetz, Joseph, Wellems, Thomas E, Wendler, Jason, White, Nicholas J, Whitton, Georgia, Yavo, William, Van Der Pluijm, Rob W, Amenga-Etego, Lucas [0000-0003-4468-0506], Anderson, Tim [0000-0002-0191-0204], Ansah, Patrick O [0000-0002-3214-5621], Ashley, Elizabeth [0000-0002-7620-4822], Ba, Hampate [0000-0002-9299-5775], Baraka, Vito [0000-0001-9694-9293], Bejon, Philip [0000-0002-2135-7549], Bertin, Gwladys I [0000-0002-2218-9591], Boni, Maciej F [0000-0002-0830-9630], Bousema, Teun [0000-0003-2666-094X], Chookajorn, Thanat [0000-0003-2876-6203], Claessens, Antoine [0000-0002-4277-0914], Conway, David J [0000-0002-8711-3037], Craig, Alister [0000-0003-0914-6164], D'Alessandro, Umberto [0000-0001-6341-5009], Day, Nicholas [0000-0003-2309-1171], Diakite, Mahamadou [0000-0002-4268-8857], Djimde, Abdoulaye [0000-0003-0062-2283], Dondorp, Arjen [0000-0001-5190-2395], Drakeley, Chris [0000-0003-4863-075X], Echeverry, Diego F [0000-0003-0301-4478], Erko, Berhanu [0000-0003-1685-752X], Faiz, Abdul [0000-0002-3460-7535], Fanello, Caterina A [0000-0003-1932-9562], Gamboa, Dionicia [0000-0002-1420-7729], Golassa, Lemu [0000-0002-1216-8711], Healy, Sara Anne [0000-0003-3078-6094], Ishengoma, Deus [0000-0003-2040-3416], Jackson, Scott A [0000-0002-3172-1607], Kamaliddin, Claire [0000-0001-8198-6235], Kamau, Edwin [0000-0002-5761-7883], Konate, Drissa S [0000-0002-4177-9642], Kwiatkowski, Dominic P [0000-0002-5023-0176], Kyle, Dennis [0000-0002-0238-965X], Lawniczak, Mara [0000-0002-3006-2080], Loua, Kovana M [0000-0003-0571-0944], Marsh, Kevin [0000-0001-8377-5466], Mayxay, Mayfong [0000-0002-6056-4516], Miotto, Olivo [0000-0001-8060-6771], Mita, Toshihiro [0000-0001-8180-2344], Mobegi, Victor [0000-0002-1962-5583], Morang'a, Collins Misita [0000-0002-6988-150X], Nguyen, Thuy-Nhien [0000-0002-4101-5706], Nosten, Francois [0000-0002-7951-0745], Ntui, Vincent Ntui-Njock [0000-0002-7532-9930], Oduro, Abraham [0000-0002-4191-7419], Onyamboko, Marie A [0000-0002-7501-5931], Ouedraogo, Jean-Bosco [0000-0003-0412-8733], Oyebola, Kolapo [0000-0002-1003-2570], Pearson, Richard [0000-0002-7386-3566], Phyo, Aung P [0000-0002-0383-9624], Price, Ric N [0000-0003-2000-2874], Rayner, Julian C [0000-0002-9835-1014], Rosanas-Urgell, Anna [0000-0002-0432-5203], Shayo, Alex [0000-0002-7099-8537], Su, Xin-Zhuan [0000-0003-3246-3248], Vinetz, Joseph [0000-0001-8344-2004], Wellems, Thomas E [0000-0003-3899-8454], and Apollo - University of Cambridge Repository

Subjects
data resource, plasmodium falciparum, genomics, malaria, genomic epidemiology
Abstract

We describe the MalariaGEN Pf7 data resource, the seventh release of Plasmodium falciparum genome variation data from the MalariaGEN network. It comprises over 20,000 samples from 82 partner studies in 33 countries, including several malaria endemic regions that were previously underrepresented. For the first time we include dried blood spot samples that were sequenced after selective whole genome amplification, necessitating new methods to genotype copy number variations. We identify a large number of newly emerging crt mutations in parts of Southeast Asia, and show examples of heterogeneities in patterns of drug resistance within Africa and within the Indian subcontinent. We describe the profile of variations in the C-terminal of the csp gene and relate this to the sequence used in the RTS,S and R21 malaria vaccines. Pf7 provides high-quality data on genotype calls for 6 million SNPs and short indels, analysis of large deletions that cause failure of rapid diagnostic tests, and systematic characterisation of six major drug resistance loci, all of which can be freely downloaded from the MalariaGEN website.

Published
2023

12. Pf7: an open dataset of Plasmodium falciparum genome variation in 20,000 worldwide samples

Author

Abdel Hamid, Muzamil Mahdi, Abdelraheem, Mohamed Hassan, Acheampong, Desmond Omane, Ahouidi, Ambroise, Ali, Mozam, Almagro-Garcia, Jacob, Amambua-Ngwa, Alfred, Amaratunga, Chanaki, Amenga-Etego, Lucas, Andagalu, Ben, Anderson, Tim, Andrianaranjaka, Voahangy, Aniebo, Ifeyinwa, Aninagyei, Enoch, Ansah, Felix, Ansah, Patrick, Apinjoh, Tobias, Arnaldo, Paulo, Ashley, Elizabeth, Auburn, Sarah, Awandare, Gordon, Ba, Hampate, Baraka, Vito, Barry, Alyssa, Bejon, Philip, Bertin, Gwladys, Boni, Maciej, Borrmann, Steffen, Bousema, Teun, Bouyou-Akotet, Marielle, Branch, Oralee, Bull, Peter, Cheah, Huch, Chindavongsa, Keobouphaphone, Chookajorn, Thanat, Chotivanich, Kesinee, Claessens, Antoine, Conway, David, Corredor, Vladimir, Courtier, Erin, Craig, Alister, d'Alessandro, Umberto, Dama, Souleymane, Day, Nicholas, Denis, Brigitte, Dhorda, Mehul, Diakite, Mahamadou, Djimde, Abdoulaye, Dolecek, Christiane, Dondorp, Arjen, Doumbia, Seydou, Drakeley, Chris, Drury, Eleanor, Duffy, Patrick, Echeverry, Diego, Egwang, Thomas, Enosse, Sonia Maria Mauricio, Erko, Berhanu, Fairhurst, Rick, Faiz, Abdul, Fanello, Caterina, Fleharty, Mark, Forbes, Matthew, Fukuda, Mark, Gamboa, Dionicia, Ghansah, Anita, Golassa, Lemu, Goncalves, Sonia, Harrison, G, Healy, Sara Anne, Hendry, Jason, Hernandez-Koutoucheva, Anastasia, Hien, Tran Tinh, Hill, Catherine, Hombhanje, Francis, Hott, Amanda, Htut, Ye, Hussein, Mazza, Imwong, Mallika, Ishengoma, Deus, Jackson, Scott, Jacob, Chris, Jeans, Julia, Johnson, Kimberly, Kamaliddin, Claire, Kamau, Edwin, Keatley, Jon, Kochakarn, Theerarat, Konate, Drissa, Konaté, Abibatou, Kone, Aminatou, Kwiatkowski, Dominic, Kyaw, Myat, Kyle, Dennis, Lawniczak, Mara, Lee, Samuel, Lemnge, Martha, Lim, Pharath, Lon, Chanthap, Loua, Kovana, Mandara, Celine, Marfurt, Jutta, Marsh, Kevin, Maude, Richard James, Mayxay, Mayfong, Maïga-Ascofaré, Oumou, Miotto, Olivo, Mita, Toshihiro, Mobegi, Victor, Mohamed, Abdelrahim Osman, Mokuolu, Olugbenga, Montgomery, Jaqui, Morang'A, Collins Misita, Mueller, Ivo, Murie, Kathryn, Newton, Paul, Ngo Duc, Thang, Nguyen, Thuy, Nguyen, Thuy-Nhien, Nguyen Thi Kim, Tuyen, Nguyen Van, Hong, Noedl, Harald, Nosten, François, Noviyanti, Rintis, Ntui, Vincent Ntui-Njock, Nzila, Alexis, Ochola-Oyier, Lynette Isabella, Ocholla, Harold, Oduro, Abraham, Omedo, Irene, Onyamboko, Marie, Ouedraogo, Jean-Bosco, Oyebola, Kolapo, Oyibo, Wellington Aghoghovwia, Pearson, Richard, Peshu, Norbert, Phyo, Aung, Plowe, Christopher, Price, Ric, Pukrittayakamee, Sasithon, Quang, Huynh Hong, Randrianarivelojosia, Milijaona, Rayner, Julian, Ringwald, Pascal, Rosanas-Urgell, Anna, Rovira-Vallbona, Eduard, Ruano-Rubio, Valentin, Ruiz, Lastenia, Saunders, David, Shayo, Alex, Siba, Peter, Simpson, Victoria, Sissoko, Mahamadou, Smith, Christen, Su, Xin-Zhuan, Sutherland, Colin, Takala-Harrison, Shannon, Talman, Arthur, Tavul, Livingstone, Thanh, Ngo Viet, Thathy, Vandana, Thu, Aung Myint, Toure, Mahamoudou, Tshefu, Antoinette, Verra, Federica, Vinetz, Joseph, Wellems, Thomas, Wendler, Jason, White, Nicholas, Whitton, Georgia, Yavo, William, van der Pluijm, Rob, MalariaGEN, University of Khartoum, University of Cape Coast [Ghana], Université Cheikh Anta Diop [Dakar, Sénégal] (UCAD), The Wellcome Trust Sanger Institute [Cambridge], London School of Hygiene and Tropical Medicine [Fajara, Gambia], London School of Hygiene and Tropical Medicine (LSHTM), National Institute of Allergy and Infectious Diseases [Bethesda] (NIAID-NIH), National Institutes of Health [Bethesda] (NIH), West African Centre for Cell Biology of Infectious Pathogens [Legon, Ghana] (WACCBIP), University of Ghana, Navrongo Health Research Centre [Navrongo, Ghana] (NHRC), Kenya Medical Research Institute (KEMRI), Texas Biomedical Research Institute [San Antonio, TX], Université d'Antananarivo, University of Buéa, Instituto Nacional de Saude [Maputo, Mozambique] (INS), Centre for Tropical Medicine and Global Health [Oxford, UK], Nuffield Department of Medicine [Oxford, UK] (Big Data Institute), University of Oxford-University of Oxford, Mahidol Oxford Tropical Medicine Research Unit (MORU), University of Oxford-Mahidol University [Bangkok]-Wellcome Trust, Menzies School of Health Research [Australia], Charles Darwin University [Australia], Nuffield Department of Clinical Medicine [Oxford], University of Oxford, Institut de Recherche pour le Développement (IRD), Laboratory of Pathogen and Host Immunity [Montpellier] (LPHI), Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM), Maladies infectieuses et vecteurs : écologie, génétique, évolution et contrôle (MIVEGEC), and Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD [France-Sud])-Université de Montpellier (UM)

Subjects
data resource, lnfectious Diseases and Global Health Radboud Institute for Health Sciences [Radboudumc 4], plasmodium falciparum, genomics, malaria, Medicine (miscellaneous), genomic epidemiology, General Biochemistry, Genetics and Molecular Biology, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract

Contains fulltext : 291985.pdf (Publisher’s version ) (Open Access) We describe the MalariaGEN Pf7 data resource, the seventh release of Plasmodium falciparum genome variation data from the MalariaGEN network. It comprises over 20,000 samples from 82 partner studies in 33 countries, including several malaria endemic regions that were previously underrepresented. For the first time we include dried blood spot samples that were sequenced after selective whole genome amplification, necessitating new methods to genotype copy number variations. We identify a large number of newly emerging crt mutations in parts of Southeast Asia, and show examples of heterogeneities in patterns of drug resistance within Africa and within the Indian subcontinent. We describe the profile of variations in the C-terminal of the csp gene and relate this to the sequence used in the RTS,S and R21 malaria vaccines. Pf7 provides high-quality data on genotype calls for 6 million SNPs and short indels, analysis of large deletions that cause failure of rapid diagnostic tests, and systematic characterisation of six major drug resistance loci, all of which can be freely downloaded from the MalariaGEN website.

Published
2023

13. A Plasmodium falciparum RING Finger E3 Ubiquitin Ligase Modifies the Roles of PfMDR1 and PfCRT in Parasite Drug Responses

Author

Singh, Brajesh K., primary, Zhang, Cui, additional, Wu, Jian, additional, Peng, Yu-Chih, additional, He, Xiao, additional, Tumas, Keyla C., additional, Sá, Juliana M., additional, Lane, Kristin D., additional, Eastman, Richard T., additional, Narum, David L., additional, Wellems, Thomas E., additional, and Su, Xin-zhuan, additional

Published
2023
Full Text
View/download PDF

15. Activation of cGAS‐STING by Lethal Malaria N67C Dictates Immunity and Mortality through Induction of CD11b+Ly6Chi Proinflammatory Monocytes

Author

Du, Yang, primary, Luo, Yien, additional, Hu, Zhiqiang, additional, Lu, Jiansen, additional, Liu, Xin, additional, Xing, Changsheng, additional, Wu, Jian, additional, Duan, Tianhao, additional, Chu, Junjun, additional, Wang, Helen Y., additional, Su, Xin‐zhuan, additional, Yu, Xiao, additional, and Wang, Rong‐Fu, additional

Published
2022
Full Text
View/download PDF

16. Additional file 7 of Multicohort transcriptome analysis of whole blood identifies robust human response signatures in Plasmodium falciparum infections

Author

Zhang, Yan-hui, Su, Xin-zhuan, Li, Jian, Shi, Jia-jian, and Xie, Li-hua

Abstract

Additional file 7: Figure S7. Immunophenotyping of whole-blood samples in malaria-infected and uninfected groups in GSE117613 datasets based on ssGSEA. The ssGSEA scores (enrichment level) were compared between noninfected and malaria-infected groups in each dataset. The statistical analyses were performed using the unpaired t-test. * p

Published
2022
Full Text
View/download PDF

17. Additional file 3 of Multicohort transcriptome analysis of whole blood identifies robust human response signatures in Plasmodium falciparum infections

Author

Zhang, Yan-hui, Su, Xin-zhuan, Li, Jian, Shi, Jia-jian, and Xie, Li-hua

Abstract

Additional file 3: FigureS3. Functional enrichment of upregulated genes and downregulated genes in the M1 module. A, GO enrichment analysis of upregulated genes. B, GO enrichment analysis of downregulated genes. 'Gene ratio' is the percentage of total DEGs in the given GO term. The size of the dots represents the number of genes in DEGs associated with the GO term and the colour of the dots represents the P-adjusted values.

Published
2022
Full Text
View/download PDF

18. Additional file 2 of Multicohort transcriptome analysis of whole blood identifies robust human response signatures in Plasmodium falciparum infections

Author

Zhang, Yan-hui, Su, Xin-zhuan, Li, Jian, Shi, Jia-jian, and Xie, Li-hua

Abstract

Additional file 2: Figure S2. Genes in M2 modules. M2 module of DEGs was identified using Molecular Complex Detection (MCODE) plug-in in Cytoscape. Genes in red indicate upregulated genes, while genes in blue indicate downregulated genes in the malaria-infected group compared to the noninfected group.

Published
2022
Full Text
View/download PDF

19. Additional file 5 of Multicohort transcriptome analysis of whole blood identifies robust human response signatures in Plasmodium falciparum infections

Author

Zhang, Yan-hui, Su, Xin-zhuan, Li, Jian, Shi, Jia-jian, and Xie, Li-hua

Abstract

Additional file 5: FigureS5. GO enrichment of highly conserved modules between malaria-infected groups of GSE117613 and GSE34404 datasets analysed using multicohort WGCNA. A, GO enrichment of blue module. B, GO enrichment of turquoise module. C, GO enrichment of brown module. D, GO enrichment of yellow module. 'Gene ratio' is the percentage of total DEGs in the given GO term. The size of the dots represents the number of genes in DEGs associated with the GO term and the colour of the dots represents the P-adjusted values.

Published
2022
Full Text
View/download PDF

20. Additional file 8 of Multicohort transcriptome analysis of whole blood identifies robust human response signatures in Plasmodium falciparum infections

Author

Zhang, Yan-hui, Su, Xin-zhuan, Li, Jian, Shi, Jia-jian, and Xie, Li-hua

Abstract

Additional file 8: Figure S8. Immunophenotyping of whole-blood samples in the mild and severe malaria group in GSE35858 datasets based on ssGSEA. The ssGSEA scores (enrichment level) were compared between the mild malaria group and severe malaria group in each dataset. The statistical analyses were performed using the unpaired t-test. * p

Published
2022
Full Text
View/download PDF

22. Additional file 4 of Multicohort transcriptome analysis of whole blood identifies robust human response signatures in Plasmodium falciparum infections

Author

Zhang, Yan-hui, Su, Xin-zhuan, Li, Jian, Shi, Jia-jian, and Xie, Li-hua

Abstract

Additional file 4: Figure.S4. GO enrichment of highly conserved modules between noninfected groups of GSE117613 and GSE34404 datasets analysed by multicohort WGCNA. A, GO enrichment of red module. B, GO enrichment of green module. 'Gene ratio' is the percentage of total DEGs in the given GO term. The size of the dots represents the number of genes in DEGs associated with the GO term and the colour of the dots represents the P-adjusted values.

Published
2022
Full Text
View/download PDF

23. Additional file 6 of Multicohort transcriptome analysis of whole blood identifies robust human response signatures in Plasmodium falciparum infections

Author

Zhang, Yan-hui, Su, Xin-zhuan, Li, Jian, Shi, Jia-jian, and Xie, Li-hua

Abstract

Additional file 6: FigureS6. Immunophenotyping of whole-blood samples in malaria-infected and uninfected groups in GSE1124 datasets based on ssGSEA. The ssGSEA scores (enrichment level) were compared between noninfected and malaria-infected groups in each dataset. The statistical analyses were performed using the unpaired t-test. * p

Published
2022
Full Text
View/download PDF

24. Additional file 1 of Multicohort transcriptome analysis of whole blood identifies robust human response signatures in Plasmodium falciparum infections

Author

Zhang, Yan-hui, Su, Xin-zhuan, Li, Jian, Shi, Jia-jian, and Xie, Li-hua

Abstract

Additional file 1: FigureS1. The receiver operating characteristic (ROC) curves of DEG expression in differentiating the malaria-infected group from the noninfected group in discovery cohorts GSE117613, GSE1124-GPL96, and GSE34404 and validation cohort GSE35858.

Published
2022
Full Text
View/download PDF

26. Activation of cGAS‐STING by Lethal Malaria N67C Dictates Immunity and Mortality through Induction of CD11b+Ly6Chi Proinflammatory Monocytes.

Author

Du, Yang, Luo, Yien, Hu, Zhiqiang, Lu, Jiansen, Liu, Xin, Xing, Changsheng, Wu, Jian, Duan, Tianhao, Chu, Junjun, Wang, Helen Y., Su, Xin‐zhuan, Yu, Xiao, and Wang, Rong‐Fu

Subjects
MYELOID differentiation factor 88, MALARIA, MONOCYTES, IMMUNITY, NATURAL immunity, PLASMODIUM yoelii, IMMUNE response
Abstract

Cyclic GMP‐AMP synthase (cGAS) and stimulator of interferon genes (STING) play critical roles in the innate immunity against infectious diseases and are required to link pathogen DNA sensing to immune responses. However, the mechanisms by which cGAS‐STING‐induced cytokines suppress the adaptive immune response against malaria infections remain poorly understood. Here, cGAS‐STING signaling is identified to play a detrimental role in regulating anti‐malaria immunity. cGAS or STING deficiency in mice markedly prolongs mouse survival during lethal malaria Plasmodium yoelii nigeriensis N67C infections by reducing late interleukin (IL)‐6 production. Mechanistically, cGAS/STING recruits myeloid differentiation factor 88 (MyD88) and specifically induces the p38‐dependent signaling pathway for late IL‐6 production, which, in turn, expands CD11b+Ly6Chi proinflammatory monocytes to inhibit immunity. Moreover, the blockage or ablation of the cGAS‐STING‐MyD88‐p38‐IL‐6 signaling axis or the depletion of CD11b+Ly6Chi proinflammatory monocytes provides mice a significant survival benefit during N67C and other lethal malaria‐strain infections. Taken together, these findings identify a previously unrecognized detrimental role of cGAS‐STING‐MyD88‐p38 axis in infectious diseases through triggering the late IL‐6 production and proinflammatory monocyte expansion and provide insight into how targeting the DNA sensing pathway, dysregulated cytokines, and proinflammatory monocytes enhances immunity against infection. [ABSTRACT FROM AUTHOR]

Published
2022
Full Text
View/download PDF

27. NAD activates olfactory receptor 1386 to regulate type I interferon responses in Plasmodium yoelii YM infection.

Author

Peng YC, Wu J, He X, Dai J, Xia L, Valenzuela-Leon P, Tumas KC, Singh BK, Xu F, Ganesan S, Munir S, Calvo E, Huang R, Liu C, Long CA, and Su XZ

Subjects
Animals, Mice, Humans, HEK293 Cells, Mice, Knockout, Signal Transduction, Mice, Inbred C57BL, Plasmodium yoelii, Malaria immunology, Malaria parasitology, Malaria metabolism, Receptors, Odorant genetics, Receptors, Odorant metabolism, Interferon Type I metabolism, Interferon Type I immunology
Abstract

Olfactory receptors (Olfr) are G protein-coupled receptors that are normally expressed on olfactory sensory neurons to detect volatile chemicals or odorants. Interestingly, many Olfrs are also expressed in diverse tissues and function in cell-cell recognition, migration, and proliferation as well as immune responses and disease processes. Here, we showed that many Olfr genes were expressed in the mouse spleen, linked to Plasmodium yoelii genetic loci significantly, and/or had genome-wide patterns of LOD scores (GPLSs) similar to those of host Toll-like receptor genes. Expression of specific Olfr genes such as Olfr1386 in HEK293T cells significantly increased luciferase signals driven by IFN-β and NF-κB promoters, with elevated levels of phosphorylated TBK1, IRF3, P38, and JNK. Mice without Olfr1386 were generated using the CRISPR/Cas9 method, and the Olfr1386 -/- mice showed significantly lower IFN-α/β levels and longer survival than wild-type (WT) littermates after infection with P. yoelii YM parasites. Inhibition of G protein signaling and P38 activity could affect cyclic AMP-responsive element promoter-driven luciferase signals and IFN-β mRNA levels in HEK293T cells expressing the Olfr1386 gene, respectively. Screening of malaria parasite metabolites identified nicotinamide adenine dinucleotide (NAD) as a potential ligand for Olfr1386, and NAD could stimulate IFN-β responses and phosphorylation of TBK1 and STAT1/2 in RAW264.7 cells. Additionally, parasite RNA (pRNA) could significantly increase Olfr1386 mRNA levels. This study links multiple Olfrs to host immune response pathways, identifies a candidate ligand for Olfr1386, and demonstrates the important roles of Olfr1386 in regulating type I interferon (IFN-I) responses during malaria parasite infections., Competing Interests: Competing interests statement:The authors declare no competing interest.

Published
2024
Full Text
View/download PDF

28. Epitranscriptome profiling of spleen mRNA m 6 A methylation reveals pathways of host responses to malaria parasite infection.

Author

Wang L, Wu J, Liu R, Chen W, Pang Z, Zhou F, Xia L, Huang J, Pan T, Su XZ, and Wang X

Subjects
Animals, Immunity, Mammals genetics, Methylation, RNA metabolism, RNA, Messenger genetics, RNA, Messenger metabolism, Spleen metabolism, Malaria, Plasmodium yoelii
Abstract

N 6 -Methyladenosine (m 6 A), the most abundant mammalian mRNA modification, has been reported to modulate various viral infections. Although it has been confirmed that RNA modifications can also modulate the replication and development of different parasites, the role of the RNA epitranscriptome in the regulation of host response post parasite infection remains to be elucidated. Here we report host spleen m 6 A epitranscriptome landscapes induced by different strains of the malaria parasite Plasmodium yoelii . We found that malaria parasite infection dramatically changes host spleen m 6 A mRNA modification and gene expression. Additionally, malaria parasite infection reprograms host immune response pathways by regulating the m 6 A modification enzymes. Collectively, our study is the first characterization of host spleen m 6 A methylome triggered by malaria parasite infections, and our data identify m 6 A modifications as significant transcriptome-wide marks during host-parasite interactions. We demonstrate that host mRNA methylation machinery can sense and respond to malaria parasite infections, and provide new insights into epitranscriptomic mechanisms underlying parasite-induced pathogenesis., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Wang, Wu, Liu, Chen, Pang, Zhou, Xia, Huang, Pan, Su and Wang.)

Published
2022
Full Text
View/download PDF

29. Activation of cGAS-STING by Lethal Malaria N67C Dictates Immunity and Mortality through Induction of CD11b + Ly6C hi Proinflammatory Monocytes.

Author

Du Y, Luo Y, Hu Z, Lu J, Liu X, Xing C, Wu J, Duan T, Chu J, Wang HY, Su XZ, Yu X, and Wang RF

Subjects
Animals, DNA, Interleukin-6 metabolism, Membrane Proteins genetics, Membrane Proteins metabolism, Mice, Myeloid Differentiation Factor 88 metabolism, Nucleotidyltransferases genetics, Nucleotidyltransferases metabolism, Malaria immunology, Malaria mortality, Monocytes immunology
Abstract

Cyclic GMP-AMP synthase (cGAS) and stimulator of interferon genes (STING) play critical roles in the innate immunity against infectious diseases and are required to link pathogen DNA sensing to immune responses. However, the mechanisms by which cGAS-STING-induced cytokines suppress the adaptive immune response against malaria infections remain poorly understood. Here, cGAS-STING signaling is identified to play a detrimental role in regulating anti-malaria immunity. cGAS or STING deficiency in mice markedly prolongs mouse survival during lethal malaria Plasmodium yoelii nigeriensis N67C infections by reducing late interleukin (IL)-6 production. Mechanistically, cGAS/STING recruits myeloid differentiation factor 88 (MyD88) and specifically induces the p38-dependent signaling pathway for late IL-6 production, which, in turn, expands CD11b + Ly6C hi proinflammatory monocytes to inhibit immunity. Moreover, the blockage or ablation of the cGAS-STING-MyD88-p38-IL-6 signaling axis or the depletion of CD11b + Ly6C hi proinflammatory monocytes provides mice a significant survival benefit during N67C and other lethal malaria-strain infections. Taken together, these findings identify a previously unrecognized detrimental role of cGAS-STING-MyD88-p38 axis in infectious diseases through triggering the late IL-6 production and proinflammatory monocyte expansion and provide insight into how targeting the DNA sensing pathway, dysregulated cytokines, and proinflammatory monocytes enhances immunity against infection., (© 2022 The Authors. Advanced Science published by Wiley-VCH GmbH.)

Published
2022
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results