RESUMEN
Non-communicable chronic diseases (NCDs) are the most widespread cause of mortality worldwide. Intestinal microbiota balance can be altered by changes in the abundance and/or diversity of intestinal microbiota, indicating a role of intestinal microbiota in NCD development. This review discusses the findings of in vitro studies, pre-clinical studies and clinical trials on the effects of Brazilian native fruits, their by-products, as well as their bioactive compounds on human intestinal microbiota and NCD. The major bioactive compounds in Brazilian native fruits and their by-products, and the impacts of their administration on outcomes linked to intestinal microbiota modulation are discussed. Mechanisms of intestinal microbiota affecting NCD could be linked to the modulation of absorption and energy balance, immune and endocrine systems, and inflammatory response. Brazilian native fruits, such as acerola, açaí, baru, buriti, guava, jabuticaba, juçara, and passion fruit, have several bioactive compounds, soluble and insoluble fibers, and a variety of phenolic compounds, which are capable of changing these key mechanisms. Brazilian native fruits and their by-products can help to promote positive intestinal and systemic health benefits by driving alterations in the composition of the human intestinal microbiota, and increasing the production of distinct short-chain fatty acids and phenolic metabolites, thereby enhancing intestinal integrity and homeostasis. Evidence from available literature shows that the modulatory impacts of Brazilian native fruits and their by-products on the composition and metabolic activity of the intestinal microbiota could improve several clinical repercussions associated with NCD, reinforcing the influence of intestinal microbiota in extra-intestinal outcomes.
RESUMEN
This study evaluated the effects of a phenolic-rich extract from jabuticaba [Myrciaria jaboticaba (Vell.) Berg] depulping waste (PEJ) on the survival, antibiotic susceptibility, virulence, and cellular functions of various enterotoxigenic Escherichia coli (ETEC) strains. The minimum inhibitory concentration of PEJ against the five tested ETEC strains was 125 mg mL-1. PEJ at 125 and 250 mg mL-1 caused reductions in viable cell counts of ≥ 3 and ≥ 5 log CFU mL-1 in ETEC over 24 h, respectively. PEJ at subinhibitory concentrations (31.25 and 62.5 mg mL-1) reduced the viable cell counts of ETEC when exposed to in vitro gastrointestinal conditions, besides decreasing the biofilm formation, cell surface hydrophobicity, mucin adhesion, and swimming and swarming motility. PEJ (31.25 and 62.5 mg mL-1) increased the susceptibility of the tested ETEC strains to various clinically relevant antibiotics. The exposure to PEJ (62.5 and 125 mg mL-1) impaired the membrane permeability and enzymatic and efflux pump activities in ETEC cells. PEJ effectively reduces survival, increases antibiotic susceptibility, and attenuates virulence in ETEC. These effects could be linked to a PEJ multi-target action disturbing various cellular functions in ETEC cells. PEJ could be a candidate for developing innovative solutions to prevent and treat ETEC infections.
