Article
Immunology
Yanbing Qiu, Yumei Huang, Meilin Chen, Yuqin Yang, Xiaoxu Li, Wenling Zhang
Summary: NLRP3 inflammasome is an intracellular polyprotein complex that is activated by perceiving different molecular patterns. Intracellular mtDNA and extracellular mtDNA have different functions in activating NLRP3 inflammasome.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2022)
Article
Medicine, Research & Experimental
Ching-Chun Yang, Chih-Hsing Wu, Ta-Chun Lin, Yi-Ning Cheng, Chin-Sung Chang, Kuo-Ting Lee, Pei-Jane Tsai, Yau-Sheng Tsai
Summary: The study reveals an additional anti-inflammatory role for PPAR gamma in suppressing NLRP3 inflammasome activation through interaction with NLRP3.
Article
Biochemistry & Molecular Biology
Huijeong Ahn, Gilyoung Lee, Byung-Cheol Han, Seung-Ho Lee, Geun-Shik Lee
Summary: This study found that maltol can inhibit the activation of inflammasomes, thus reducing inflammation. By inhibiting ROS production and Casp1 activity, maltol exerts its anti-inflammatory effects.
Article
Multidisciplinary Sciences
Fabian A. Fischer, Linda F. M. Mies, Sohaib Nizami, Eirini Pantazi, Sara Danielli, Benjamin Demarco, Michael Ohlmeyer, Michelle Sue Jann Lee, Cevayir Coban, Jonathan C. Kagan, Elena Di Daniel, Jelena S. Bezbradica
Summary: The activation of NLRP3 inflammasome is regulated by multiple mechanisms, including a posttranslational phospho-switch described in this study. This phospho-switch involves the protein phosphatase 2A (PP2A) as an ON switch and the kinases TANK-binding kinase 1 (TBK1) and I-kappa-B kinase epsilon (IKKe) as an OFF switch. Understanding these regulatory mechanisms could provide new insights for disease interventions related to NLRP3 activation.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
(2021)
Article
Multidisciplinary Sciences
Inga Hochheiser, Michael Pilsl, Gregor Hagelueken, Jonas Moecking, Michael Marleaux, Rebecca Brinkschulte, Eicke Latz, Christoph Engel, Matthias Geyer
Summary: This study determined the conformational states of human NLRP3 and its interaction with the inhibitor CRID3 through cryo-electron microscopy. The findings provide insights into the regulatory mechanism of NLRP3 and offer potential for the treatment of related diseases.
Article
Biochemistry & Molecular Biology
Meng Song, Zijun Chen, Ruian Qiu, Tingwei Zhi, Wenmin Xie, Yingya Zhou, Nachuan Luo, Fuqian Chen, Fang Liu, Chuangpeng Shen, Sheng Lin, Fengxue Zhang, Yong Gao, Changhui Liu
Summary: Excessive accumulation of bile acids (BA) in hepatocytes triggers inflammatory response and recruitment of macrophages, accelerating cholestatic liver injury. This study reveals the importance of crosstalk between hepatocytes and macrophages in the pathogenesis of cholestasis and suggests that blocking this crosstalk by inhibiting NLRP3 inflammasome activation may be a novel therapeutic strategy for cholestasis.
Review
Immunology
Han Cheng, Lingling Chen, Minchun Huang, Jin Hou, Zhifeng Chen, Xiaojun Yang
Summary: NLRP3 inflammasome plays a key role in radiation-induced tissue injury, but its potential value is not adequately recognized. Early intervention/prevention strategies targeting NLRP3 inflammasome may help resolve clinical problems caused by radiation.
FRONTIERS IN IMMUNOLOGY
(2022)
Article
Immunology
Yuhua Shi, Qian Lv, Mengjie Zheng, Hongxiang Sun, Fushan Shi
Summary: INF39 is a specific inhibitor for NLRP3 inflammasome activation, without affecting other inflammasomes. It exerts its anti-inflammatory effect by inhibiting the interaction of NEK7-NLRP3 and other downstream events.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2021)
Article
Immunology
Ruijie Dong, Zhenyi Xue, Guangyue Fan, Na Zhang, Chengzhi Wang, Guangliang Li, Yurong Da
Summary: Pin1 regulates NLRP3 inflammasome activation through the p38 MAPK signaling pathway in mice, impacting shock mortality and organ damage. Lack of Pin1 reduces NLRP3 inflammasome activation and secretion of inflammatory cytokines, suggesting Pin1 as a potential target for treating inflammatory diseases such as septic shock.
FRONTIERS IN IMMUNOLOGY
(2021)
Article
Cell Biology
Huijeong Ahn, Gilyoung Lee, Jeongeun Kim, Jeongho Park, Seung Goo Kang, Sung-Il Yoon, Eunsong Lee, Geun-Shik Lee
Summary: NLRP3 inflammasome activation inhibits LCN2 secretion while inducing IL-1β in mouse macrophages. The inhibition of NLRP3 triggers on LCN2 secretion is caused by the inhibited transcription and translation of LCN2, suggesting a new linkage between inflammasome activation and LCN2 secretion in the innate immunity.
Article
Nanoscience & Nanotechnology
Dipika Nandi, Manisha Shivrayan, Jingjing Gao, Jithu Krishna, Ritam Das, Bin Liu, S. Thayumanavan, Ashish Kulkarni
Summary: Designer nanomaterials capable of delivering immunomodulators to specific immune cells have been extensively studied, but certain nanomaterials can nonspecifically activate NLRP3 inflammasomes, leading to unwanted effects. Core hydrophobicity strongly activates NLRP3 assembly compared to other nanoparticle attributes. Different signaling pathways and kinetics are observed with varying core hydrophobicity patterns.
ACS APPLIED MATERIALS & INTERFACES
(2021)
Article
Immunology
Yingting Hou, Hongbin He, Ming Ma, Rongbin Zhou
Summary: NLRP3 is an important innate immune sensor that activates the inflammasome complex, resulting in the secretion of IL-1 beta and pyroptosis. The mechanism of NLRP3 inflammasome activation in response to crystals or particulates is unclear, but lysosomal damage has been implicated. This study discovered that apilimod, a lysosomal disruptor, is a selective and potent NLRP3 agonist that triggers mitochondrial damage and lysosomal dysfunction, leading to NLRP3 inflammasome activation.
FRONTIERS IN IMMUNOLOGY
(2023)
Article
Chemistry, Multidisciplinary
Mei-yue Song, Jia-xin Wang, You-liang Sun, Zhi-fa Han, Yi-tian Zhou, Ying Liu, Tian-hui Fan, Zhao-guo Li, Xian-mei Qi, Ya Luo, Pei-ran Yang, Bai-cun Li, Xin-ri Zhang, Jing Wang, Chen Wang
Summary: This study established silicosis mouse models to investigate the effectiveness of tetrandrine in early and late therapeutic administration, revealing its novel mechanism of attenuating silicosis by inhibiting the NLRP3 inflammasome pathways in lung macrophages. The findings not only demonstrated promising results against silicosis-associated inflammation and fibrosis, but also laid the groundwork for understanding the molecular targets of tetrandrine, potentially leading to a globally accepted therapeutic strategy for silicosis.
ACTA PHARMACOLOGICA SINICA
(2022)
Article
Neurosciences
Nikhil Panicker, Tae-In Kam, Hu Wang, Stewart Neifert, Shih-Ching Chou, Manoj Kumar, Saurav Brahmachari, Aanishaa Jhaldiyal, Jared T. Hinkle, Fatih Akkentli, Xiaobo Mao, Enquan Xu, Senthilkumar S. Karuppagounder, Eric T. Hsu, Sung-Ung Kang, Olga Pletnikova, Juan Troncoso, Valina L. Dawson, Ted M. Dawson
Summary: Parkinson's disease is caused by alpha-synuclein accumulation and death of dopamine neurons in the substantia nigra pars compacta, with NLRP3 inflammasome hyperactivation playing a role in the disease. Loss of parkin activity leads to spontaneous assembly of NLRP3 inflammasome in dopamine neurons, which is further exacerbated by mitochondrial-derived reactive oxygen species. Inhibition of neuronal NLRP3 inflammasome assembly can prevent degeneration of dopamine neurons in PD models.
Article
Virology
Yanqi Wang, Zhirong Sun, Hongkai Zhang, Yahui Song, Yi Wang, Wei Xu, Min Li
Summary: The study reveals that coxsackievirus B3 infection inhibits the activation of the NLRP3 inflammasome in macrophages by suppressing the NF-κB signaling pathway and ROS production, resulting in decreased IL-1β production and increased susceptibility to Escherichia coli infection. These findings provide new ideas for antiviral treatment and drug development against coxsackievirus B3 infection.
Article
Cell Biology
M. P. Cabral-Piccin, L. V. C. Guillermo, N. S. Vellozo, A. A. Filardy, S. T. Pereira-Marques, T. S. Rigoni, W. F. Pereira-Manfro, G. A. DosReis, M. F. Lopes
CELL DEATH & DISEASE
(2016)
Article
Immunology
Natalia S. Vellozo, Samara T. Pereira-Marques, Mariela P. Cabral-Piccin, Alessandra A. Filardy, Flavia L. Ribeiro-Gomes, Thais S. Rigoni, George A. DosReis, Marcela F. Lopes
FRONTIERS IN IMMUNOLOGY
(2017)
Article
Immunology
Kamila Guimaraes-Pinto, Danielle Oliveira Nascimento, Antonia Correa-Ferreira, Alexandre Morrot, Celio G. Freire-de-Lima, Marcela F. Lopes, George A. DosReis, Alessandra A. Filardy
FRONTIERS IN IMMUNOLOGY
(2018)
Review
Oncology
Alexandre Morrot, Leonardo Marques da Fonseca, Eduardo J. Salustiano, Luciana Boffoni Gentile, Luciana Conde, Alessandra Almeida Filardy, Tatiany Nunes Franklim, Kelli Monteiro da Costa, Celio Geraldo Freire-de-Lima, Leonardo Freire-de-Lima
FRONTIERS IN ONCOLOGY
(2018)
Review
Immunology
Alessandra Almeida Filardy, Kamila Guimaraes-Pinto, Marise Pinheiro Nunes, Ketiuce Zukeram, Lara Fliess, Ludimila Pereira, Danielle Oliveira Nascimento, Luciana Conde, Alexandre Morrot
FRONTIERS IN IMMUNOLOGY
(2018)
Article
Immunology
Thais S. Rigoni, Natalia S. Vellozo, Mariela Cabral-Piccin, Laryssa Fabiano-Coelho, Ulisses G. Lopes, Alessandra A. Filardy, George A. DosReis, Marcela F. Lopes
FRONTIERS IN IMMUNOLOGY
(2020)
Article
Oncology
Natalia Rodrigues Mantuano, Michal A. Stanczak, Isadora de Araujo Oliveira, Nicole Kirchhammer, Alessandra A. Filardy, Gianni Monaco, Ronan Christian Santos, Agatha Carlos Fonseca, Miguel Fontes, Cesar de Souza Bastos, Wagner B. Dias, Alfred Zippelius, Adriane R. Todeschini, Heinz Laeubli
CANCER IMMUNOLOGY RESEARCH
(2020)
Article
Immunology
Angelica Arcanjo, Kamila Guimaraes Pinto, Jorgete Logullo, Paulo Emilio Correa Leite, Camilla Cristie Barreto Menezes, Leonardo Freire-de-Lima, Israel Diniz-Lima, Debora Decote-Ricardo, Rodrigo Nunes Rodrigues-da-Silva, Celio Geraldo Freire-de-Lima, Alessandra Almeida Filardy, Josue da Costa Lima-Junior, Alvaro Luiz Bertho, Paula Mello De Luca, Jose Mauro Granjeiro, Shana Priscila Coutinho Barroso, Fatima Conceicao-Silva, Wilson Savino, Alexandre Morrot
Summary: The study reveals that COVID-19 patients experience abnormal cytokine response and T cell abnormalities, including an increased proportion of effector exhausted/senescent cells. The deficiency in CD4(+) T cells, which play a crucial role in immune response, may lead to loss of clonal repertoire and susceptibility to viral relapse.
JOURNAL OF INFECTIOUS DISEASES
(2021)
Article
Immunology
Kamila Guimaraes-Pinto, Ester P. Maia, Jesuino R. M. Ferreira, Alessandra A. Filardy
Summary: Efferocytosis is crucial for maintaining lung homeostasis and controlling inflammation. Lung macrophages recognize signals on apoptotic cells to control immune responses, prevent excessive inflammation, and autoimmunity. Abnormalities in efferocytosis can contribute to the pathophysiology of chronic inflammatory lung diseases and affect susceptibility or resistance to pulmonary microbial infections.
IMMUNOLOGY LETTERS
(2022)
Article
Biology
Thais S. Rigoni, Natalia S. Vellozo, Kamila Guimaraes-Pinto, Mariela Cabral-Piccin, Laryssa Fabiano-Coelho, Thayane C. Matos-Silva, Alessandra A. Filardy, Christina M. Takiya, Marcela F. Lopes
Summary: Axl receptor participates in the efferocytosis of apoptotic lymphocytes during Trypanosoma cruzi infection, impacting macrophage-mediated immunity. Axl(-/-) macrophages enhance M1 responses induced by immune T cells and improve parasite infection and cardiac inflammation.
COMMUNICATIONS BIOLOGY
(2022)
Review
Infectious Diseases
Kamila Guimaraes-Pinto, Jesuino R. M. Ferreira, Andre L. A. da Costa, Alexandre Morrot, Leonardo Freire-de-Lima, Debora Decote-Ricardo, Celio Geraldo Freire-de-Lima, Alessandra A. Filardy
Summary: Chagas disease is a neglected tropical disease caused by Trypanosoma cruzi infection. Excessive immune system stimulation driven by parasite persistence may lead to the deterioration of immune functions and the progression of Chagas disease. Understanding the chronic inflammatory status induced by T. cruzi and its effects on host defense capacity could provide insights for developing therapeutic approaches for the prevention and treatment of Chagas disease.
TROPICAL MEDICINE AND INFECTIOUS DISEASE
(2022)
Review
Infectious Diseases
Ana Caroline Costa-da-Silva, Danielle de Oliveira Nascimento, Jesuino R. M. Ferreira, Kamila Guimaraes-Pinto, Leonardo Freire-de-Lima, Alexandre Morrot, Debora Decote-Ricardo, Alessandra Almeida Filardy, Celio Geraldo Freire-de-Lima
Summary: Leishmaniasis is a widespread and neglected parasitic disease caused by various species of Leishmania, with severity depending on multiple factors. This article discusses the role of the immune system, its molecules, and responses in the development of Leishmaniasis, focusing on the interactions between innate immune cells and Leishmania major.
TROPICAL MEDICINE AND INFECTIOUS DISEASE
(2022)
Meeting Abstract
Immunology
Kamila Guimaraes Pinto, Antonia Castro Ferreira, Monique Leandro, Marcela F. Lopes, Estefania Vazquez, JianPing He, Brian L. Kelsall, Alessandra Filardy
JOURNAL OF IMMUNOLOGY
(2020)
Meeting Abstract
Oncology
Natalia Rodrigues Mantuano, Michal Stanczak, Isadora Oliveira, Alessandra Filardy, Ronan Silva, Alfred Zippelius, Adriane Regina Todeschini, Heinz Laubli