Autor(es)

Machado, Melissa S. G. ; Rodrigues, Vanessa F. ; Barbosa, Sara C. ; Elias-Oliveira, Jefferson ; Pereira, italo S. ; Pereira, Jessica A. ; Pacheco, Thailla C. F. ; Carlos, Daniela

• Tipo de documento: Artigo Científico
• Fonte: MICROORGANISMS; v. 12, n. 8, p. 14-pg., 2024-08-01.

Resumo

Intestinal permeability and bacterial translocation are increased in obesity and metabolic syndrome (MS). ILC3 cells contribute to the integrity of intestinal epithelium by producing IL-22 via IL-1 beta and IL-23. This study investigates the role of IL-1R1 in inducing ILC3 cells and conferring protection during obesity and MS. For this purpose, C57BL/6 wild-type (WT) and IL-1R1-deficient mice were fed a standard diet (SD) or high-fat diet (HFD) for 16 weeks. Weight and blood glucose levels were monitored, and adipose tissue and blood samples were collected to evaluate obesity and metabolic parameters. The small intestine was collected to assess immunological and junction protein parameters through flow cytometry and RT-PCR, respectively. The intestinal permeability was analyzed using the FITC-dextran assay. The composition of the gut microbiota was also analyzed by qPCR. We found that IL-1R1 deficiency exacerbates MS in HFD-fed mice, increasing body fat and promoting glucose intolerance. A worsening of MS in IL-1R1-deficient mice was associated with a reduction in the ILC3 population in the small intestine. In addition, we found decreased IL-22 expression, increased intestinal permeability and bacterial translocation to the visceral adipose tissue of these mice compared to WT mice. Thus, the IL-1R1 receptor plays a critical role in controlling intestinal homeostasis and obesity-induced MS, possibly through the differentiation or activation of IL-22-secreting ILC3s. (AU)

• Processo FAPESP: 18/14815-0 - Estudo do perfil do microbioma intestinal e do potencial terapêutico de estratégias de intervenção na imunopatogenia do Diabetes tipo 1 e 2
• Beneficiário: Daniela Carlos Sartori
• Modalidade de apoio: Auxílio à Pesquisa - Jovens Pesquisadores - Fase 2
• Processo FAPESP: 22/06787-1 - Contribuição da IL-1 na ativação e função de células ILC3 na mucosa intestinal durante a síndrome metabólica induzida por obesidade
• Beneficiário: Melissa Santana Gonsalez Machado
• Modalidade de apoio: Bolsas no Brasil - Iniciação Científica