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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

CD36 Shunts Eicosanoid Metabolism to Repress CD14 Licensed Interleukin-1 beta Release and Inflammation

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Author(s):
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Zoccal, Karina F. [1] ; Gardinassi, Luiz G. [1] ; Sorgi, Carlos A. [1] ; Meirelles, Alyne F. G. [1] ; Bordon, Karla C. F. [2] ; Glezer, Isaias [3] ; Cupo, Palmira [4] ; Matsuno, Alessandra K. [4] ; Bollela, Valdes R. [5] ; Arantes, Eliane C. [2] ; Guimaraes, Francisco S. [6] ; Faccioli, Lucia Helena [1]
Total Authors: 12
Affiliation:
[1] Univ Sao Paulo, Fac Ciencias Farmaceut Ribeirao Preto, Dept Anal Clin Toxicol & Bromatol, Ribeirao Preto - Brazil
[2] Univ Sao Paulo, Fac Ciencias Farmaceut Ribeirao Preto, Dept Fis & Quim, Ribeirao Preto - Brazil
[3] Univ Fed Sao Paulo, Escola Paulista Med, Dept Bioquim, Sao Paulo - Brazil
[4] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Puericultura & Pediat, Ribeirao Preto - Brazil
[5] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Clin Med, Ribeirao Preto - Brazil
[6] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Farmacol, Ribeirao Preto - Brazil
Total Affiliations: 6
Document type: Journal article
Source: FRONTIERS IN IMMUNOLOGY; v. 9, APR 27 2018.
Web of Science Citations: 4
Abstract

Interleukin (IL)-1 beta is a potential target for treatment of several inflammatory diseases, including envenomation by the scorpion Tityus serrulatus. In this context, bioactive lipids such as prostaglandin (PG)E-2 and leukotriene (LT)B-4 modulate the production of IL-1 beta by innate immune cells. Pattern recognition receptors (PRRs) that perceive T. serrulatus venom (TsV), and orchestrate LTB4, PGE(2), and cyclic adenosine monophosphate (cAMP) production to regulate IL-1 beta release are unknown. Furthermore, molecular mechanisms driving human cell responses to TsV remain uncharacterized. Here, we identified that both CD14 and CD36 control the synthesis of bioactive lipids, inflammatory cytokines, and mortality mediated by TsV. CD14 induces PGE(2)/cAMP/IL-1 beta release and inflammation. By contrast, CD36 shunts eicosanoid metabolism toward production of LTB4, which represses the PGE(2)/cAMP/IL-1 beta axis and mortality. Of importance, the molecular mechanisms observed in mice strongly correlate with those of human cell responses to TsV. Overall, this study provides major insights into molecular mechanisms connecting CD14 and CD36 with differential eicosanoid metabolism and inflammation mediated by IL-1 beta. (AU)

FAPESP's process: 14/03332-7 - Study of the relationship between inflammasome activation and lipid mediators production with pulmonary inflammation induced by scorpion venom with and without hyaluronidase
Grantee:Karina Furlani Zoccal
Support type: Scholarships in Brazil - Post-Doctorate
FAPESP's process: 14/07125-6 - New functional aspects of eicosanoids
Grantee:Lúcia Helena Faccioli
Support type: Research Projects - Thematic Grants
FAPESP's process: 13/07937-8 - Redoxome - Redox Processes in Biomedicine
Grantee:Ohara Augusto
Support type: Research Grants - Research, Innovation and Dissemination Centers - RIDC
FAPESP's process: 15/00658-1 - New functional aspects of eicosanoids
Grantee:Lúcia Helena Faccioli
Support type: Multi-user Equipment Program