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3. Tuberculosis: Integrated Studies for a Complex Disease 2050

Author

Rezaei, Nima, Hosseini, Nastaran-Sadat, Saghazadeh, Amene, Fateh, Abolfazl, Duse, Adriano, Ahmad, Aijaz, Braley, Alexander E., Tahta, Alican, Kamboj, Alisha, Khan, Amer Hayat, Coelho, Ana Cláudia, Fuso, Andrea, Varón, Andrés, Trajman, Anete, Saxena, Anil Kumar, Ganeshpurkar, Ankit, Casapao, Anthony M., Tkachenko, Anton, Devnikar, Anushka V., Moshiri, Arfa, Muñoz-Barrutia, Arrate, Dasgupta, Arunava, Natarajan, Arvind, Gupta, Ashish, Coyne, Ashlan J. Kunz, Jordan, Ashly E., Kumar, Ashok, Ergeshov, Atadzhan, Pourakbari, Babak, Joshi, Basant, Chavarro-Portillo, Bibiana, Soto, Carlos Y., Kanipe, Carly, Schmidt, Christiane Mello, Cox, Christophe, Gómez-Cruz, Clara, Cardoso, Claudete Aparecida Araújo, Sant´Anna, Clemax Couto, Johnson, Courtney, Rodríguez-Silva, Cristhian N., Rosales, Cristian, Licona-Cassani, Cuauhtémoc, Fast, Cynthia D., Pérez-Martínez, Damián, Pizzol, Damiano, Perlman, David C., Philips, Dennis, Viveros, Diana, Fisher, Dina A., Butov, Dmytro, Egelund, Eric F., de Igartua, Everest, Bhatt, Garima, Mgode, Georgies, Quaglio, Gianluca, Putoto, Giovanni, Mini, G. K., Thomas-Richardson, Govind, Wylie, Greg, dos Santos Fernandes, Guilherme Felipe, Bermúdez, Gustavo, Quintas, Hélder, Verma, Himanshu, Eoh, Hyungjin, Putera, Ikhwanuliman, Sivokozov, Ilya, Pires, Isabel, Lee, Jae Jin, Lombard, Jason E., dos Santos, Jean Leandro, Zellweger, Jean-Pierre, Thomas-Richardson, Jenu, Lordson, Jinbert, Prates, João Lucas, Cervantes, Jorge, Porcel, José M., Vaquero, Juan José, Prada, Justina, Kamboj, Kamal, Tabbara, Khalid F., Mussie, Kirubel Manyazewal, Patel, Krupesh, Porcel, Laura, Fiebig, Lena, Mohan, Malu, Yadav, Mange Ram, López-R, Marcela, Correia-Neves, Margarida, da Conceição Fontes, Maria, de Fátima Pombo Bazhuni Sant´Anna, Maria, Cañadas-Ortega, Marina, Singh, Meenakshi, Lause, Michael, Maya-Hoyos, Milena, Omrani, Mir Davood, Palmer, Mitchell V., Ahmad, Mohammad Naiyaz, Seid, Mohammed Assen, Chauhan, Monica, Saxena, Mridula, Marimani, Musa, Srinivas, Nanduri, Beyene, Negussie, Arenas, Nelson E., Cardoso, Nicole, Oliveira, Olena, Silakari, Om, Inlamea, Osvaldo, Tanrıverdi, Özgür, Boggiatto, Paola M., Santos, Paola, Mejía-Ponce, Paulina, Soares, Pedro, Sell, Philip, Murumkar, Prashant R., Devanandan, Praveen, Zheng, Qi, Lim, Rachel K., Aurílio, Rafaela Baroni, Ghuge, Rahul B., Barot, Rahul R., Rahul, Puvvada, Ranadheer Chowdary, Duarte, Raquel, Singh, Ravi, Sinha, Richa, La Distia Nora, Rina, Burny, Robert, Zenteno-Cuevas, Roberto, Mali, Sagar, Shoughy, Samir S., Tarashi, Samira, Mishra, Sapna, Malasala, Satyaveni, Mamishi, Setareh, Siadat, Seyed Davar, Choudhary, Shalki, Mahmoudi, Shima, Chopra, Sidharth, Nandi, Sisir, Faisal, Sobia, Goel, Sonu, Huszár, Stanislav, Field, Stephen K., Singh, Sushil Kumar, Rito, Teresa, Butova, Tetiana, Manning, Thomas, van der Werf, Tjip S., Myasoedov, Valeriy, Vásquez, Vanessa, Muthukumar, Vijey Aanandhi, Singh, Vinayak, Hall, Walter A., Hikmahwati, Wandya, Turgut, Yaşar Barış, Thaker, Yatri, Kawabata, Yoshinori, de Reus, Yvette A., and Rezaei, Nima, Editor-in-Chief

Published
2023
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10. Targeting Mycobacterium tuberculosis Persistence through Inhibition of the Trehalose Catalytic Shift

Author

Kalera, Karishma, primary, Liu, Rachel, additional, Lim, Juhyeon, additional, Pathirage, Rasangi, additional, Swanson, Daniel H., additional, Johnson, Ulysses G., additional, Stothard, Alicyn I., additional, Lee, Jae Jin, additional, Poston, Anne W., additional, Woodruff, Peter J., additional, Ronning, Donald R., additional, Eoh, Hyungjin, additional, and Swarts, Benjamin M., additional

Published
2024
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12. TXNIP-mediated crosstalk between oxidative stress and glucose metabolism

Author

Kim, Stephanie, primary, Ge, Jianning, additional, Kim, Dokyun, additional, Lee, Jae Jin, additional, Choi, Youn Jung, additional, Chen, Weiqiang, additional, Bowman, James W., additional, Foo, Suan-Sin, additional, Chang, Lin-Chun, additional, Liang, Qiming, additional, Hara, Daiki, additional, Choi, Inpyo, additional, Kim, Myung Hee, additional, Eoh, Hyungjin, additional, and Jung, Jae U., additional

Published
2024
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14. Hepatitis B virus e antigen induces atypical metabolism and differentially regulates programmed cell deaths of macrophages.

Author

Li, Yumei, Wu, Christine, Lee, Jiyoung, Ning, Qiqi, Lim, Juhyeon, Eoh, Hyungjin, Wang, Sean, Hurrell, Benjamin P., Akbari, Omid, and Ou, Jing-hsiung James

Subjects
HEPATITIS E virus, HEPATITIS B virus, APOPTOSIS, KREBS cycle, MACROPHAGES
Abstract

Macrophages can undergo M1-like proinflammatory polarization with low oxidative phosphorylation (OXPHOS) and high glycolytic activities or M2-like anti-inflammatory polarization with the opposite metabolic activities. Here we show that M1-like macrophages induced by hepatitis B virus (HBV) display high OXPHOS and low glycolytic activities. This atypical metabolism induced by HBV attenuates the antiviral response of M1-like macrophages and is mediated by HBV e antigen (HBeAg), which induces death receptor 5 (DR5) via toll-like receptor 4 (TLR4) to induce death-associated protein 3 (DAP3). DAP3 then induces the expression of mitochondrial genes to promote OXPHOS. HBeAg also enhances the expression of glutaminases and increases the level of glutamate, which is converted to α-ketoglutarate, an important metabolic intermediate of the tricarboxylic acid cycle, to promote OXPHOS. The induction of DR5 by HBeAg leads to apoptosis of M1-like and M2-like macrophages, although HBeAg also induces pyroptosis of the former. These findings reveal novel activities of HBeAg, which can reprogram mitochondrial metabolism and trigger different programmed cell death responses of macrophages depending on their phenotypes to promote HBV persistence. Author summary: Hepatitis B virus (HBV) causes chronic infection in approximately 300 million people in the world, resulting in nearly 1 million deaths per year. How HBV establishes chronic infection in patients is an interesting question. Hepatic macrophages play important role in HBV clearance and persistence. They can be induced by external stimuli to display different metabolic activities. Here we demonstrates that HBV can reprogram the metabolism of macrophages to induce oxidative phosphorylation to attenuate their anti-HBV activities and in the meantime differentially regulate programmed cell deaths of macrophages based on their phenotypes. These results provide important information for understanding the mechanism of HBV persistence and pathogenesis and offer a new avenue for the development of novel treatments for HBV patients. [ABSTRACT FROM AUTHOR]

Published
2024
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16. Publisher Correction: Multi-omic analysis of selectively vulnerable motor neuron subtypes implicates altered lipid metabolism in ALS

Author

Lee, Hojae, Lee, Jae Jin, Park, Na Young, Dubey, Sandeep Kumar, Kim, Taeyong, Ruan, Kai, Lim, Su Bin, Park, Seong-Hyun, Ha, Shinwon, Kovlyagina, Irina, Kim, Kyung-tai, Kim, Seongjun, Oh, Yohan, Kim, Hyesoo, Kang, Sung-Ung, Song, Mi-Ryoung, Lloyd, Thomas E., Maragakis, Nicholas J., Hong, Young Bin, Eoh, Hyungjin, and Lee, Gabsang

Published
2022
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28. Arginine-mediated gut microbiome remodeling promotes host pulmonary immune defense against nontuberculous mycobacterial infection

Author

Kim, Young Jae, primary, Lee, June-Young, additional, Lee, Jae Jin, additional, Jeon, Sang Min, additional, Silwal, Prashanta, additional, Kim, In Soo, additional, Kim, Hyeon Ji, additional, Park, Cho Rong, additional, Chung, Chaeuk, additional, Han, Jeong Eun, additional, Choi, Jee-Won, additional, Tak, Euon Jung, additional, Yoo, Ji-Ho, additional, Jeong, Su-Won, additional, Kim, Do-Yeon, additional, Ketphan, Warisa, additional, Kim, Su-Young, additional, Jhun, Byung Woo, additional, Whang, Jake, additional, Kim, Jin-Man, additional, Eoh, Hyungjin, additional, Bae, Jin-Woo, additional, and Jo, Eun-Kyeong, additional

Published
2022
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31. Publisher Correction: Multi-omic analysis of selectively vulnerable motor neuron subtypes implicates altered lipid metabolism in ALS

Author

Lee, Hojae, primary, Lee, Jae Jin, additional, Park, Na Young, additional, Dubey, Sandeep Kumar, additional, Kim, Taeyong, additional, Ruan, Kai, additional, Lim, Su Bin, additional, Park, Seong-Hyun, additional, Ha, Shinwon, additional, Kovlyagina, Irina, additional, Kim, Kyung-tai, additional, Kim, Seongjun, additional, Oh, Yohan, additional, Kim, Hyesoo, additional, Kang, Sung-Ung, additional, Song, Mi-Ryoung, additional, Lloyd, Thomas E., additional, Maragakis, Nicholas J., additional, Hong, Young Bin, additional, Eoh, Hyungjin, additional, and Lee, Gabsang, additional

Published
2021
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34. Characterization of the Mycobacterium tuberculosis 4-diphosphocytidy1-2-C-methyl-D-erythritol synthase: potential for drug development

Author

Eoh, Hyungjin, Brown, Amanda C., Buetow, Lori, Hunter, William N., Parish, Tanya, Kaur, Devinder, Brennan, Patrick J., and Crick, Dean C.

Subjects
Mycobacterium tuberculosis -- Physiological aspects, Mycobacterium tuberculosis -- Genetic aspects, Bacterial genetics -- Research, Pharmaceutical research, Biological sciences
Abstract

Mycobacterium tuberculosis utilizes the methylerythritol phosphate (MEP) pathway for biosynthesis of isopentenyl diphosphate and its isomer, dimethylallyl diphosphate, precursors of all isoprenoid compounds. This pathway is of interest as a source of new drug targets, as it is absent from humans and disruption of the responsible genes has shown a lethal phenotype for Escherichia coli. In the MEP pathway, 4-diphosphocytidy1-2-C-methyl-D-erythritol is formed from 2-C-methyl-D-erythritol 4-phosphate (MEP) and CTP in a reaction catalyzed by a 4-diphosphocytidy1-2-C-methyl-D-erythritol synthase (IspD). In the present work, we demonstrate that Rv3582c is essential for M. tuberculosis: Rv3582c has been cloned and expressed, and the encoded protein has been purified. The purified M. tuberculosis IspD protein was capable of catalyzing the formation of 4-diphosphocytidy1-2-C-methyl-D-erythritol in the presence of MEP and CTP. The enzyme was active over a broad pH range (pH 6.0 to 9.0), with peak activity at pH 8.0. The activity was absolutely dependent upon divalent cations, with 20 mM [Mg.sup.2+] being optimal, and replacement of CTP with other nucleotide 5'-triphosphates did not support activity. Under the conditions tested, M. tuberculosis IspD had [K.sub.m] values of 58.5 [micro]M for MEP and 53.2 [micro]M for CTP. Calculated [k.sub.cat] and [k.sub.cat]/[K.sub.m] values were 0.72 [min.sup.-1] and 12.3 [mM.sup.-1] [min.sup.-1] for MEP and 1.0 [min.sup.-1] and 18.8 [mM.sup.-1] [min.sup.-1] for CTP, respectively.

Published
2007

36. Metabolic neutralization mitigates propionate toxicity in intracellular Mycobacterium tuberculosis

Author

Lee, Jae Jin, Lim, Juhyeon, Gao, Shengjia, Lawson, Christopher, Odell, Mark, Raheem, Saki, Woo, JeongIm, Kang, Sung-Ho, Jeon, Bo-Young, and Eoh, Hyungjin

Subjects
C500 Microbiology, C521 Medical Microbiology, food and beverages, C530 Bacteriology, C730 Metabolic Biochemistry, C510 Applied Microbiology
Abstract

Metabolic networks in biological systems are interconnected, such that malfunctioning parts can be corrected by other parts within the network, a process termed adaptive metabolism. Unlike Bacillus Calmette-Guérin (BCG), Mycobacterium tuberculosis (Mtb) better manages its intracellular lifestyle by executing adaptive metabolism. Here, we used metabolomics and identified glutamate synthase (GltB/D) that converts glutamine to glutamate (Q → E) as a metabolic effort used to neutralize cytoplasmic pH that is acidified while consuming host propionate carbon through the methylcitrate cycle (MCC). Methylisocitrate lyase, the last step of the MCC, is intrinsically downregulated in BCG, leading to obstruction of carbon flux toward central carbon metabolism, accumulation of MCC intermediates, and interference with GltB/D mediated neutralizing activity against propionate toxicity. Indeed, vitamin B12 mediated bypass MCC and additional supplement of glutamate led to selectively correct the phenotypic attenuation in BCG and restore the adaptive capacity of BCG to the similar level of Mtb phenotype. Collectively, a defective crosstalk between MCC and Q → E contributes to attenuation of intracellular BCG. Furthermore, GltB/D inhibition enhances the level of propionate toxicity in Mtb. Thus, these findings revealed a new adaptive metabolism and propose GltB/D as a synergistic target to improve the antimicrobial outcomes of MCC inhibition in Mtb.

Published
2018

37. Inhibiting the stringent response blocks Mycobacterium tuberculosis entry into quiescence and reduces persistence

Author

Dutta, Noton K., primary, Klinkenberg, Lee G., additional, Vazquez, Maria-Jesus, additional, Segura-Carro, Delfina, additional, Colmenarejo, Gonzalo, additional, Ramon, Fernando, additional, Rodriguez-Miquel, Beatriz, additional, Mata-Cantero, Lydia, additional, Porras-De Francisco, Esther, additional, Chuang, Yu-Min, additional, Rubin, Harvey, additional, Lee, Jae Jin, additional, Eoh, Hyungjin, additional, Bader, Joel S., additional, Perez-Herran, Esther, additional, Mendoza-Losana, Alfonso, additional, and Karakousis, Petros C., additional

Published
2019
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38. Regulation of Polar Peptidoglycan Biosynthesis by Wag31 Phosphorylation in Mycobacteria

Author

Lee Sang, Suh Joo-Won, Lee Jung-Yeon, Nyayapathy Seeta, Han Jeong-Sun, Sahana Moodakare, Hamasha Khozima, Lee Jae, Eoh Hyungjin, Jani Charul, Rehse Steve J, Crick Dean C, and Kang Choong-Min

Subjects
Microbiology, QR1-502
Abstract

Abstract Background Sensing and responding to environmental changes is a central aspect of cell division regulation. Mycobacterium tuberculosis contains eleven Ser/Thr kinases, two of which, PknA and PknB, are key signaling molecules that regulate cell division/morphology. One substrate of these kinases is Wag31, and we previously showed that partial depletion of Wag31 caused morphological changes indicative of cell wall defects, and that the phosphorylation state of Wag31 affected cell growth in mycobacteria. In the present study, we further characterized the role of the Wag31 phosphorylation in polar peptidoglycan biosynthesis. Results We demonstrate that the differential growth among cells expressing different wag31 alleles (wild-type, phosphoablative, or phosphomimetic) is caused by, at least in part, dissimilar nascent peptidoglycan biosynthesis. The phosphorylation state of Wag31 is found to be important for protein-protein interactions between the Wag31 molecules, and thus, for its polar localization. Consistent with these results, cells expressing a phosphomimetic wag31 allele have a higher enzymatic activity in the peptidoglycan biosynthetic pathway. Conclusions The Wag31Mtb phosphorylation is a novel molecular mechanism by which Wag31Mtb regulates peptidoglycan synthesis and thus, optimal growth in mycobacteria.

Published
2010
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45. Ergothioneine Maintains Redox and Bioenergetic Homeostasis Essential for Drug Susceptibility and Virulence of Mycobacterium tuberculosis

Author

Saini, Vikram, primary, Cumming, Bridgette M., additional, Guidry, Loni, additional, Lamprecht, Dirk A., additional, Adamson, John H., additional, Reddy, Vineel P., additional, Chinta, Krishna C., additional, Mazorodze, James H., additional, Glasgow, Joel N., additional, Richard-Greenblatt, Melissa, additional, Gomez-Velasco, Anaximandro, additional, Bach, Horacio, additional, Av-Gay, Yossef, additional, Eoh, Hyungjin, additional, Rhee, Kyu, additional, and Steyn, Adrie J.C., additional

Published
2016
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49. Δ20 IFITM2 differentially restricts X4 and R5 HIV-1.

Author

Wan-Lin Wu, Grotefend, Christopher Robert, Ming-Ting Tsai, Yi-Ling Wang, Radic, Vladimir, Eoh, Hyungjin, and I-Chueh Huang

Subjects
CXCR4 receptors, PROTEIN receptors, MEDICAL microbiology, PROTEOMICS, VIROCAP (Medical test), INFECTION
Abstract

CCR5 (R5)-tropic, but not CXCR4 (X4)-tropic, HIV-1 is associated with primary HIV-1 infection and transmission. Recent studies have shown that IFN-induced transmembrane (IFITM) proteins, including IFITM1, IFITM2 and IFITM3, restrict a broad range of viruses. Here, we demonstrate that an IFITM2 isoform (Δ20 IFITM2) lacking 20 amino acids at the N terminus differentially restricts X4 and R5 HIV-1. Δ20 IFITM2 suppresses replication of X4 HIV-1 strains by inhibiting their entry. High levels of Δ20 IFITM2 expression could be detected in CD4+ T cells and in monocytes. Infection of X4 viruses in monocyte-derived macrophages and dendritic cells is enhanced upon depletion of IFITM2 isoforms. Furthermore, we also show that coreceptor use is the determining factor for differential HIV-1 restriction of Δ20 IFITM2. When we replace the C terminus of CCR5 with the C terminus of CXCR4, R5 viruses become more susceptible to Δ20 IFITM2-mediated restriction. In contrast to previous studies, our research reveals that neither X4 nor R5 HIV-1 is suppressed by IFITM2 and IFITM3. The multifactor gatekeeping model has been proposed to explain restriction of X4 viruses in the early stage of HIV-1 diseases. Our findings indicate that Δ20 IFITM2 may serve as a major contributor to this gatekeeping mechanism. [ABSTRACT FROM AUTHOR]

Published
2017
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