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NLRX1 modulates differentially NLRP3 inflammasome activation and NF-κB signaling during Fusobacterium nucleatum infection.
Hung, Shu-Chen; Huang, Pei-Rong; Almeida-da-Silva, Cássio Luiz Coutinho; Atanasova, Kalina R; Yilmaz, Ozlem; Ojcius, David M.
Afiliación
  • Hung SC; Department of Biomedical Sciences, University of the Pacific, Arthur A. Dugoni School of Dentistry, San Francisco, CA 94103, USA.
  • Huang PR; Center for Molecular and Clinical Immunology, Chang Gung University, Gueishan, Taoyuan 333, Taiwan, ROC.
  • Almeida-da-Silva CLC; Department of Biomedical Sciences, University of the Pacific, Arthur A. Dugoni School of Dentistry, San Francisco, CA 94103, USA; Immunobiology Program, Biophysics Institute of the Federal University of Rio de Janeiro, RJ 21941, Brazil.
  • Atanasova KR; Department of Periodontology and Emerging Pathogens Institute, University of Florida, Gainesville, FL 32610, USA.
  • Yilmaz O; Department of Oral Health Sciences, Medical University of South Carolina, Charleston, SC, USA; Department of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, USA.
  • Ojcius DM; Department of Biomedical Sciences, University of the Pacific, Arthur A. Dugoni School of Dentistry, San Francisco, CA 94103, USA. Electronic address: dojcius@pacific.edu.
Microbes Infect ; 20(9-10): 615-625, 2018.
Article en En | MEDLINE | ID: mdl-29024797
NOD-like receptors (NLRs) play a large role in regulation of host innate immunity, yet their role in periodontitis remains to be defined. NLRX1, a member of the NLR family that localizes to mitochondria, enhances mitochondrial ROS (mROS) generation. mROS can activate the NLRP3 inflammasome, yet the role of NLRX1 in NLRP3 inflammasome activation has not been examined. In this study, we revealed the mechanism by which NLRX1 positively regulates ATP-induced NLRP3 inflammasome activation through mROS in gingival epithelial cells (GECs). We found that depletion of NLRX1 by shRNA attenuated ATP-induced mROS generation and redistribution of the NLRP3 inflammasome adaptor protein, ASC. Furthermore, depletion of NLRX1 inhibited Fusobacterium nucleatum infection-activated caspase-1, suggesting that it also inhibits the NLRP3 inflammasome. Conversely, NLRX1 also acted as a negative regulator of NF-κB signaling and IL-8 expression. Thus, NLRX1 stimulates detection of the pathogen F. nucleatum via the inflammasome, while dampening cytokine production. We expect that commensals should not activate the inflammasome, and NLRX1 should decrease their ability to stimulate expression of pro-inflammatory cytokines such as IL-8. Therefore, NLRX1 may act as a potential switch with regards to anti-microbial responses in healthy or diseased states in the oral cavity.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Transducción de Señal / Proteínas Mitocondriales / Factor de Transcripción ReIA / Inflamasomas / Proteína con Dominio Pirina 3 de la Familia NLR / Infecciones por Fusobacterium Límite: Humans Idioma: En Revista: Microbes Infect Asunto de la revista: ALERGIA E IMUNOLOGIA / MICROBIOLOGIA Año: 2018 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Francia
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Transducción de Señal / Proteínas Mitocondriales / Factor de Transcripción ReIA / Inflamasomas / Proteína con Dominio Pirina 3 de la Familia NLR / Infecciones por Fusobacterium Límite: Humans Idioma: En Revista: Microbes Infect Asunto de la revista: ALERGIA E IMUNOLOGIA / MICROBIOLOGIA Año: 2018 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Francia