|Support type:||Scholarships in Brazil - Post-Doctorate|
|Effective date (Start):||September 01, 2019|
|Effective date (End):||August 31, 2021|
|Field of knowledge:||Health Sciences - Medicine|
|Principal Investigator:||Eliana Pereira de Araujo|
|Home Institution:||Faculdade de Enfermagem. Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil|
|Associated research grant:||13/07607-8 - OCRC - Obesity and Comorbidities Research Center, AP.CEPID|
In the past few decades, the study of Brown Adipose Tissue (BAT) thermogenesis in adult human brought new insights to the problem of obesity. The presence of this tissue in newborn was already known and its importance to maintain body temperature and survival are undeniable. A recent study from our group demonstrated that mice lacking IL10, an anti-inflammatory cytokine, are incapable to respond to cold due to mitochondrial defects on BAT. Humans that have deficiency in IL10 also exhibit similar mitochondrial problems. In this context, SIDS (Sudden Infant Death Syndrome) is an important cause of death in newborns during the first year of life and can be defined as death with not known cause even after thorough investigation. Despite the efforts to unravel its cause, the mechanisms leading to SIDS remain unclear. A study published recently described immunological polymorphisms in SIDS cases and found strong association between IL10 gene variations and the disease. To address this issue, our aim is to evaluate the importance of IL10 in body temperature regulation both in human newborns and mouse model. Besides that, explore therapeutic strategies to increase BAT function to overlap IL10 absence, perhaps through CD1, an immune molecule recently described as a BAT activator and immunological regulator in the central nervous system.