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13 results on '"Quadros, Andreza U."'

1. Anthrax toxins regulate pain signaling and can deliver molecular cargoes into ANTXR2+ DRG sensory neurons

Author

Yang, Nicole J., Isensee, Jörg, Neel, Dylan V., Quadros, Andreza U., Zhang, Han-Xiong Bear, Lauzadis, Justas, Liu, Sai Man, Shiers, Stephanie, Belu, Andreea, Palan, Shilpa, Marlin, Sandra, Maignel, Jacquie, Kennedy-Curran, Angela, Tong, Victoria S., Moayeri, Mahtab, Röderer, Pascal, Nitzsche, Anja, Lu, Mike, Pentelute, Bradley L., Brüstle, Oliver, Tripathi, Vineeta, Foster, Keith A., Price, Theodore J., Collier, R. John, Leppla, Stephen H., Puopolo, Michelino, Bean, Bruce P., Cunha, Thiago M., Hucho, Tim, and Chiu, Isaac M.

Published
2022
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2. C5aR1 signaling triggers lung immunopathology in COVID-19 through neutrophil extracellular traps

Author

Silva, Bruna M., Gomes, Giovanni F., Veras, Flavio P., Cambier, Seppe, Silva, Gabriel V.L., Quadros, Andreza U., Caetite, Diego B., Nascimento, Daniele C., Silva, Camilla M., Silva, Juliana C., Damasceno, Samara, Schneider, Ayda H., Beretta, Fabio, Batah, Sabrina S., Castro, Icaro M.S., Paiva, Isadora M., Rodrigues, Tamara, Salina, Ana, Martins, Ronaldo, Cebinelli, Guilherme C.M., Bibo, Naira L., Jorge, Daniel M., Nakaya, Helder I., Zamboni, Dario S., Leiria, Luiz O., Fabro, Alexandre T., Alves-Filho, Jose C., Arruda, Eurico, Louzada-Junior, Paulo, Oliveira, Rene D., Cunha, Larissa D., Van Mol, Pierre, Vanderbeke, Lore, Feys, Simon, Wauters, Els, Brandolini, Laura, Aramini, Andrea, Cunha, Fernando Q., Kohl, Jorg, Allegretti, Marcello, Lambrechts, Diether, Wauters, Joost, Proost, Paul, and Cunha, Thiago M.

Subjects
Cytokines -- Health aspects, Lung diseases -- Development and progression -- Risk factors, Immune response -- Health aspects, Neutrophils -- Health aspects, Cellular signal transduction -- Health aspects, Extrachromosomal DNA -- Health aspects, Immunologic diseases -- Risk factors -- Development and progression, Health care industry
Abstract

Patients with severe COVID-19 develop acute respiratory distress syndrome (ARDS) that may progress to cytokine storm syndrome, organ dysfunction, and death. Considering that complement component 5a (C5a), through its cellular receptor C5aR1, has potent proinflammatory actions and plays immunopathological roles in inflammatory diseases, we investigated whether the C5a/C5aR1 pathway could be involved in COVID-19 pathophysiology. C5a/C5aR1 signaling increased locally in the lung, especially in neutrophils of critically ill patients with COVID-19 compared with patients with influenza infection, as well as in the lung tissue of K18-hACE2 Tg mice (Tg mice) infected with SARS-CoV-2. Genetic and pharmacological inhibition of C5aR1 signaling ameliorated lung immunopathology in Tg-infected mice. Mechanistically, we found that C5aR1 signaling drives neutrophil extracellular traps-dependent (NETs-dependent) immunopathology. These data confirm the immunopathological role of C5a/C5aR1 signaling in COVID-19 and indicate that antagonists of C5aR1 could be useful for COVID-19 treatment., Introduction COVID-19 is the major acute global public health issue in this century. Patients with severe COVID-19 develop acute respiratory distress syndrome (ARDS), which may progress to organ dysfunction and [...]

Published
2023
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3. Paclitaxel binds and activates C5aR1: A new potential therapeutic target for the prevention of chemotherapy-induced peripheral neuropathy and hypersensitivity reactions

Author

Brandolini, Laura, d’Angelo, Michele, Novelli, Rubina, Castelli, Vanessa, Giorgio, Cristina, Sirico, Anna, Cocchiaro, Pasquale, D’Egidio, Francesco, Benedetti, Elisabetta, Cristiano, Claudia, Bugatti, Antonella, Ruocco, Anna, Amendola, Pier Giorgio, Talarico, Carmine, Manelfi, Candida, Iaconis, Daniela, Beccari, Andrea, Quadros, Andreza U., Cunha, Thiago M., Caruso, Arnaldo, Russo, Roberto, Cimini, Annamaria, Aramini, Andrea, and Allegretti, Marcello

Published
2022
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5. Complement receptor C5aR1 signaling in sensory neuron-associated macrophages drives neuropathic pain

Author

Quadros, Andreza U., primary, Maganin, Alexandre G. M., additional, Silva, Conceição E. A., additional, Damasceno, Samara, additional, Cavallini, Maria C. M., additional, Davoli-Ferreira, Marcela, additional, Lopes, Alexandre H. P., additional, Sagar, Devi R., additional, Brandolini, Laura, additional, Lee, Sang Hoon, additional, Alves-Filho, Jose C., additional, Cunha, Fernando Q., additional, Berta, Temugin, additional, Köhl, Jörg, additional, Allegretti, Marcello, additional, Chapman, Victoria, additional, and Cunha, Thiago M., additional

Published
2022
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6. Anthrax toxins regulate pain signaling and can deliver molecular cargoes into ANTXR2+ DRG sensory neurons

Author

Yang, Nicole J., primary, Isensee, Jörg, additional, Neel, Dylan V., additional, Quadros, Andreza U., additional, Zhang, Han-Xiong Bear, additional, Lauzadis, Justas, additional, Liu, Sai Man, additional, Shiers, Stephanie, additional, Belu, Andreea, additional, Palan, Shilpa, additional, Marlin, Sandra, additional, Maignel, Jacquie, additional, Kennedy-Curran, Angela, additional, Tong, Victoria S., additional, Moayeri, Mahtab, additional, Röderer, Pascal, additional, Nitzsche, Anja, additional, Lu, Mike, additional, Pentelute, Bradley L., additional, Brüstle, Oliver, additional, Tripathi, Vineeta, additional, Foster, Keith A., additional, Price, Theodore J., additional, Collier, R. John, additional, Leppla, Stephen H., additional, Puopolo, Michelino, additional, Bean, Bruce P., additional, Cunha, Thiago M., additional, Hucho, Tim, additional, and Chiu, Isaac M., additional

Published
2021
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7. Anthrax toxins regulate pain signaling and can deliver molecular cargoes into ANTXR2+DRG sensory neurons

Author

Yang, Nicole J., Isensee, Jörg, Neel, Dylan V., Quadros, Andreza U., Zhang, Han-Xiong Bear, Lauzadis, Justas, Liu, Sai Man, Shiers, Stephanie, Belu, Andreea, Palan, Shilpa, Marlin, Sandra, Maignel, Jacquie, Kennedy-Curran, Angela, Tong, Victoria S., Moayeri, Mahtab, Röderer, Pascal, Nitzsche, Anja, Lu, Mike, Pentelute, Bradley L., Brüstle, Oliver, Tripathi, Vineeta, Foster, Keith A., Price, Theodore J., Collier, R. John, Leppla, Stephen H., Puopolo, Michelino, Bean, Bruce P., Cunha, Thiago M., Hucho, Tim, and Chiu, Isaac M.

Abstract

Bacterial products can act on neurons to alter signaling and function. In the present study, we found that dorsal root ganglion (DRG) sensory neurons are enriched for ANTXR2, the high-affinity receptor for anthrax toxins. Anthrax toxins are composed of protective antigen (PA), which binds to ANTXR2, and the protein cargoes edema factor (EF) and lethal factor (LF). Intrathecal administration of edema toxin (ET (PA + EF)) targeted DRG neurons and induced analgesia in mice. ET inhibited mechanical and thermal sensation, and pain caused by formalin, carrageenan or nerve injury. Analgesia depended on ANTXR2 expressed by Nav1.8+or Advillin+neurons. ET modulated protein kinase A signaling in mouse sensory and human induced pluripotent stem cell-derived sensory neurons, and attenuated spinal cord neurotransmission. We further engineered anthrax toxins to introduce exogenous protein cargoes, including botulinum toxin, into DRG neurons to silence pain. Our study highlights interactions between a bacterial toxin and nociceptors, which may lead to the development of new pain therapeutics.

Published
2022
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10. Anticoagulant and fibrinogenolytic properties of the venom of Polybia occidentalis social wasp

Author

Czaikoski, Paula G, primary, Menaldo, Danilo L, additional, Marcussi, Silvana, additional, Baseggio, Anne LC, additional, Fuly, André L, additional, Paula, Rafael C, additional, Quadros, Andreza U, additional, Romão, Pedro RT, additional, Buschini, Maria LT, additional, Cunha, Fernando Q, additional, Soares, Andreimar M, additional, and Monteiro, Marta C, additional

Published
2010
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11. Anthrax toxins regulate pain signaling and can deliver molecular cargoes into ANTXR2(+) DRG sensory neurons

Author

Yang, Nicole J., Isensee, Joerg, Neel, Dylan, V, Quadros, Andreza U., Zhang, Han-Xiong Bear, Lauzadis, Justas, Liu, Sai Man, Shiers, Stephanie, Belu, Andreea, Palan, Shilpa, Marlin, Sandra, Maignel, Jacquie, Kennedy-Curran, Angela, Tong, Victoria S., Moayeri, Mahtab, Roederer, Pascal, Nitzsche, Anja, Lu, Mike, Pentelute, Bradley L., Bruestle, Oliver, Tripathi, Vineeta, Foster, Keith A., Price, Theodore J., Collier, R. John, Leppla, Stephen H., Puopolo, Michelino, Bean, Bruce P., Cunha, Thiago M., Hucho, Tim, Chiu, Isaac M., Yang, Nicole J., Isensee, Joerg, Neel, Dylan, V, Quadros, Andreza U., Zhang, Han-Xiong Bear, Lauzadis, Justas, Liu, Sai Man, Shiers, Stephanie, Belu, Andreea, Palan, Shilpa, Marlin, Sandra, Maignel, Jacquie, Kennedy-Curran, Angela, Tong, Victoria S., Moayeri, Mahtab, Roederer, Pascal, Nitzsche, Anja, Lu, Mike, Pentelute, Bradley L., Bruestle, Oliver, Tripathi, Vineeta, Foster, Keith A., Price, Theodore J., Collier, R. John, Leppla, Stephen H., Puopolo, Michelino, Bean, Bruce P., Cunha, Thiago M., Hucho, Tim, and Chiu, Isaac M.

Abstract

Discovering that nociceptive sensory neurons express the receptor for anthrax toxin, Yang et al. show that anthrax toxin can induce potent analgesia in mice and facilitate the delivery of potentially analgesic cargo proteins into nociceptive neurons. Bacterial products can act on neurons to alter signaling and function. In the present study, we found that dorsal root ganglion (DRG) sensory neurons are enriched for ANTXR2, the high-affinity receptor for anthrax toxins. Anthrax toxins are composed of protective antigen (PA), which binds to ANTXR2, and the protein cargoes edema factor (EF) and lethal factor (LF). Intrathecal administration of edema toxin (ET (PA + EF)) targeted DRG neurons and induced analgesia in mice. ET inhibited mechanical and thermal sensation, and pain caused by formalin, carrageenan or nerve injury. Analgesia depended on ANTXR2 expressed by Na(v)1.8(+) or Advillin(+) neurons. ET modulated protein kinase A signaling in mouse sensory and human induced pluripotent stem cell-derived sensory neurons, and attenuated spinal cord neurotransmission. We further engineered anthrax toxins to introduce exogenous protein cargoes, including botulinum toxin, into DRG neurons to silence pain. Our study highlights interactions between a bacterial toxin and nociceptors, which may lead to the development of new pain therapeutics.

12. Anthrax toxins regulate pain signaling and can deliver molecular cargoes into ANTXR2(+) DRG sensory neurons

Author

Yang, Nicole J., Isensee, Joerg, Neel, Dylan, V, Quadros, Andreza U., Zhang, Han-Xiong Bear, Lauzadis, Justas, Liu, Sai Man, Shiers, Stephanie, Belu, Andreea, Palan, Shilpa, Marlin, Sandra, Maignel, Jacquie, Kennedy-Curran, Angela, Tong, Victoria S., Moayeri, Mahtab, Roederer, Pascal, Nitzsche, Anja, Lu, Mike, Pentelute, Bradley L., Bruestle, Oliver, Tripathi, Vineeta, Foster, Keith A., Price, Theodore J., Collier, R. John, Leppla, Stephen H., Puopolo, Michelino, Bean, Bruce P., Cunha, Thiago M., Hucho, Tim, Chiu, Isaac M., Yang, Nicole J., Isensee, Joerg, Neel, Dylan, V, Quadros, Andreza U., Zhang, Han-Xiong Bear, Lauzadis, Justas, Liu, Sai Man, Shiers, Stephanie, Belu, Andreea, Palan, Shilpa, Marlin, Sandra, Maignel, Jacquie, Kennedy-Curran, Angela, Tong, Victoria S., Moayeri, Mahtab, Roederer, Pascal, Nitzsche, Anja, Lu, Mike, Pentelute, Bradley L., Bruestle, Oliver, Tripathi, Vineeta, Foster, Keith A., Price, Theodore J., Collier, R. John, Leppla, Stephen H., Puopolo, Michelino, Bean, Bruce P., Cunha, Thiago M., Hucho, Tim, and Chiu, Isaac M.

Abstract

Discovering that nociceptive sensory neurons express the receptor for anthrax toxin, Yang et al. show that anthrax toxin can induce potent analgesia in mice and facilitate the delivery of potentially analgesic cargo proteins into nociceptive neurons. Bacterial products can act on neurons to alter signaling and function. In the present study, we found that dorsal root ganglion (DRG) sensory neurons are enriched for ANTXR2, the high-affinity receptor for anthrax toxins. Anthrax toxins are composed of protective antigen (PA), which binds to ANTXR2, and the protein cargoes edema factor (EF) and lethal factor (LF). Intrathecal administration of edema toxin (ET (PA + EF)) targeted DRG neurons and induced analgesia in mice. ET inhibited mechanical and thermal sensation, and pain caused by formalin, carrageenan or nerve injury. Analgesia depended on ANTXR2 expressed by Na(v)1.8(+) or Advillin(+) neurons. ET modulated protein kinase A signaling in mouse sensory and human induced pluripotent stem cell-derived sensory neurons, and attenuated spinal cord neurotransmission. We further engineered anthrax toxins to introduce exogenous protein cargoes, including botulinum toxin, into DRG neurons to silence pain. Our study highlights interactions between a bacterial toxin and nociceptors, which may lead to the development of new pain therapeutics.

13. Paclitaxel binds and activates C5aR1: A new potential therapeutic target for the prevention of chemotherapy-induced peripheral neuropathy and hypersensitivity reactions

Author

Laura Brandolini, Michele d’Angelo, Rubina Novelli, Vanessa Castelli, Cristina Giorgio, Anna Sirico, Pasquale Cocchiaro, Francesco D’Egidio, Elisabetta Benedetti, Claudia Cristiano, Antonella Bugatti, Anna Ruocco, Pier Giorgio Amendola, Carmine Talarico, Candida Manelfi, Daniela Iaconis, Andrea Beccari, Andreza U. Quadros, Thiago M. Cunha, Arnaldo Caruso, Roberto Russo, Annamaria Cimini, Andrea Aramini, Marcello Allegretti, Brandolini, Laura, D'Angelo, Michele, Novelli, Rubina, Castelli, Vanessa, Giorgio, Cristina, Sirico, Anna, Cocchiaro, Pasquale, D'Egidio, Francesco, Benedetti, Elisabetta, Cristiano, Claudia, Bugatti, Antonella, Ruocco, Anna, Amendola, Pier Giorgio, Talarico, Carmine, Manelfi, Candida, Iaconis, Daniela, Beccari, Andrea, Quadros, Andreza U, Cunha, Thiago M, Caruso, Arnaldo, Russo, Roberto, Cimini, Annamaria, Aramini, Andrea, and Allegretti, Marcello

Subjects
Cancer Research, Paclitaxel, Anaphylatoxin C5a, Animal, Immunology, Peripheral Nervous System Diseases, Antineoplastic Agents, Cell Biology, Rats, Antineoplastic Agent, Molecular Docking Simulation, Mice, Cellular and Molecular Neuroscience, Hyperalgesia, Rat, Animals, Receptor, Anaphylatoxin C5a, Receptor
Abstract

Chemotherapy-induced peripheral neuropathy (CIPN) and hypersensitivity reactions (HSRs) are among the most frequent and impairing side effects of the antineoplastic agent paclitaxel. Here, we demonstrated that paclitaxel can bind and activate complement component 5a receptor 1 (C5aR1) and that this binding is crucial in the etiology of paclitaxel-induced CIPN and anaphylaxis. Starting from our previous data demonstrating the role of interleukin (IL)-8 in paclitaxel-induced neuronal toxicity, we searched for proteins that activate IL-8 expression and, by using the Exscalate platform for molecular docking simulations, we predicted the high affinity of C5aR1 with paclitaxel. By in vitro studies, we confirmed the specific and competitive nature of the C5aR1-paclitaxel binding and found that it triggers intracellularly the NFkB/P38 pathway and c-Fos. In F11 neuronal cells and rat dorsal root ganglia, C5aR1 inhibition protected from paclitaxel-induced neuropathological effects, while in paclitaxel-treated mice, the absence (knock-out mice) or the inhibition of C5aR1 significantly ameliorated CIPN symptoms—in terms of cold and mechanical allodynia—and reduced the chronic pathological state in the paw. Finally, we found that C5aR1 inhibition can counteract paclitaxel-induced anaphylactic cytokine release in macrophages in vitro, as well as the onset of HSRs in mice. Altogether these data identified C5aR1 as a key mediator and a new potential pharmacological target for the prevention and treatment of CIPN and HSRs induced by paclitaxel.

Published
2022

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