Busca avançada
Ano de início
Entree
(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

Gut Microbiome Dysbiosis and Immunometabolism: New Frontiers for Treatment of Metabolic Diseases

Texto completo
Autor(es):
Belizario, Jose E. [1] ; Faintuch, Joel [2] ; Garay-Malpartida, Miguel [3]
Número total de Autores: 3
Afiliação do(s) autor(es):
[1] Univ Sao Paulo, Inst Biomed Sci, Dept Pharmacol, BR-05508900 Sao Paulo, SP - Brazil
[2] Univ Sao Paulo, Med Sch, Dept Gastroenterol, BR-05403000 Sao Paulo, SP - Brazil
[3] Univ Sao Paulo, Sch Arts Sci & Humanities EACH, BR-03828000 Sao Paulo, SP - Brazil
Número total de Afiliações: 3
Tipo de documento: Artigo de Revisão
Fonte: Mediators of Inflammation; 2018.
Citações Web of Science: 11
Resumo

Maintenance of healthy human metabolism depends on a symbiotic consortium among bacteria, archaea, viruses, fungi, and host eukaryotic cells throughout the human gastrointestinal tract. Microbial communities provide the enzymatic machinery and the metabolic pathways that contribute to food digestion, xenobiotic metabolism, and production of a variety of bioactive molecules. These include vitamins, amino acids, short-chain fatty acids (SCFAs), and metabolites, which are essential for the interconnected pathways of glycolysis, the tricarboxylic acid/Krebs cycle, oxidative phosphorylation (OXPHOS), and amino acid and fatty acid metabolism. Recent studies have been elucidating how nutrients that fuel the metabolic processes impact on the ways immune cells, in particular, macrophages, respond to different stimuli under physiological and pathological conditions and become activated and acquire a specialized function. The two major inflammatory phenotypes of macrophages are controlled through differential consumption of glucose, glutamine, and oxygen. M1 phenotype is triggered by polarization signal from bacterial lipopolysaccharide (LPS) and Th1 proinflammatory cytokines such as interferon-gamma, TNF-alpha, and IL-1 beta, or both, whereas M2 phenotype is triggered by Th2 cytokines such as interleukin-4 and interleukin-13 as well as anti-inflammatory cytokines, IL-10 and TGF beta, or glucocorticoids. Glucose utilization and production of chemical mediators including ATP, reactive oxygen species (ROS), nitric oxide (NO), and NADPH support effector activities of M1 macrophages. Dysbiosis is an imbalance of commensal and pathogenic bacteria and the production of microbial antigens and metabolites. It is now known that the gut microbiota-derived products induce low-grade inflammatory activation of tissue-resident macrophages and contribute to metabolic and degenerative diseases, including diabetes, obesity, metabolic syndrome, and cancer. Here, we update the potential interplay of host gut microbiome dysbiosis and metabolic diseases. We also summarize on advances on fecal therapy, probiotics, prebiotics, symbiotics, and nutrients and small molecule inhibitors of metabolic pathway enzymes as prophylactic and therapeutic agents for metabolic diseases. (AU)

Processo FAPESP: 07/04513-1 - Papel da nova citocina PANDER na indução de apoptose ou proliferação celular em linhagens tumorais de próstata e de mama
Beneficiário:Humberto Miguel Garay Malpartida
Linha de fomento: Auxílio à Pesquisa - Regular
Processo FAPESP: 15/18647-6 - Human microbiomes and their roles in dysbiosis, common diseases and novel therapeutic approaches
Beneficiário:José Ernesto Belizario
Linha de fomento: Auxílio à Pesquisa - Publicações científicas - Artigo