Anti-inflammatory pathways of kefir in murine model: a systematic review.

CONTEXT: Kefir consumption has been associated with immune response modulation, antioxidant, and anti-inflammatory effects. OBJECTIVE: The objective of this systematic review was to investigate the role of kefir against inflammation and the main response mechanisms involved in this process in a murine model. DATA SOURCES: The searches were searched in the PubMed, Science Direct, and LILACS databases. Only murine model studies, according to PRISMA guidelines, published in the past 10 years were included. STUDY SELECTION: Only articles about original and placebo-controlled experiments in murine models used to investigate the anti-inflammatory mechanisms of kefir were considered. Of the articles found, 349 were excluded according to the following criteria: duplicate articles (n = 99), off-topic title and abstract (n = 157), reviews (n = 47), studies in vitro (n = 29), and studies with humans (n = 17). In total, 23 studies were included in this review. DATA EXTRACTION: Two independently working authors assessed the risk of bias and extracted data from the included studies. RESULTS: Kefir consumption had positive effects on inflammation modulation. The main mechanisms involved were the reduction of pro-inflammatory and molecular markers; reduction in inflammatory infiltrate in tissues, serum biomarkers, risk factors for chronic diseases, and parasitic infection; composition and metabolic activity change of intestinal microbiota and mycobiota; activation of humoral and cellular immunity; and modulation of oxidative stress. CONCLUSIONS: Kefir modulates the immune system in different experimental models, among other secondary outcomes, to improve overall health. The beverage reduces inflammation through the alternation between innate, Th1, and Th2 responses, reducing levels of pro-inflammatory cytokines while increasing those of anti-inflammatory ones. In addition, it also mediates immunomodulatory and protective effects through the numerous molecular biomarkers and organic acids produced and secreted by kefir in the intestinal microbiota. The health-promoting effects attributed to kefir may help in the different treatments of inflammatory, chronic, and infectious diseases in the population.

Milk kefir alters fecal microbiota impacting gut and brain health in mice.

Kefir is a fermented beverage made of a symbiotic microbial community that stands out for health benefits. Although its microbial profile is still little explored, its effects on modulation of gut microbiota and production of short-chain fatty acids (SCFAs) seems to act by improving brain health. This work aimed to analyze the microbiota profile of milk kefir and its effect on metabolism, oxidative stress, and in the microbiota-gut-brain axis in a murine model. The experimental design was carried out using C57BL-6 mice (n = 20) subdivided into groups that received 0.1 mL water or 0.1 mL (10% w/v) kefir. The kefir proceeded to maturation for 48 h, and then it was orally administered, via gavage, to the animals for 4 weeks. Physicochemical, microbiological, antioxidant analyzes, and microbial profiling of milk kefir beverage were performed as well as growth parameters, food intake, serum markers, oxidative stress, antioxidant enzymes, SCFAs, and metabarcoding were analyzed in the mice. Milk kefir had 76.64 ± 0.42% of free radical scavenging and the microbiota composed primarily by the genus Comamonas. Moreover, kefir increased catalase and superoxide dismutase (colon), and SCFAs in feces (butyrate), and in the brain (butyrate and propionate). Kefir reduced triglycerides, uric acid, and affected the microbiome of animals increasing fecal butyrate-producing bacteria (Lachnospiraceae and Lachnoclostridium). Our results on the brain and fecal SCFAs and the antioxidant effect found were associated with the change in the gut microbiota caused by kefir, which indicates that kefir positively influences the gut-microbiota-brain axis and contributes to the preservation of gut and brain health. KEY POINTS: • Milk kefir modulates fecal microbiota and SCFA production in brain and colon. • Kefir treatment increases the abundance of SCFA-producing bacteria. • Milk kefir increases antioxidant enzymes and influences the metabolism of mice.

The role of IL-10 in regulating inflammation and gut microbiome in mice consuming milk kefir and orally challenged with S. Typhimurium.

Kefir has been suggested as a possible bacterial prophylaxis against Salmonella and IL-10 production seems to be crucial in the pathogenesis of salmonellosis in mice. This study evaluated the role of IL-10 in the inflammation and gut microbiome in mice consuming milk kefir and orally challenged with Salmonella enterica serovar Typhimurium. C57BL wild type (WT) (n = 40) and C57BL IL-10-/- (KO) (n = 40) mice were subdivided into eight experimental groups either treated or not with kefir. In the first 15 days, the water groups received filtered water (0.1 mL) while the kefir groups received milk kefir (10% w/v) orally by gavage. Then, two groups of each strain received a single dose (0.1 mL) of the inoculum of S. Typhimurium (ATCC 14028, dose: 106 CFU mL-1). After four weeks, the animals were euthanized to remove the colon for further analysis. Kefir prevented systemic infections only in IL-10-/- mice, which were able to survive, regulate cytokines, and control colon inflammation. The abundance in Lachnospiraceae and Roseburia, and also the higher SCFA production in the pre-infection, showed that kefir has a role in intestinal health and protection, colonizing and offering competition for nutrients with the pathogen as well as acting in the regulation of salmonella infectivity only in the absence of IL-10. These results demonstrate the role of IL-10 in the prognosis of salmonellosis and how milk kefir can be used in acute infections.

Antioxidant potential of Buriti (Mauritia flexuosa) pulp flour in diabetic rats

Buriti pulp flour (BPF) contains significant levels of antioxidants. This study evaluated the effect of BPF on biomarkers of oxidative damage in the liver, heart, and pancreas of diabetic rats. The chemical composition, antioxidant capacity, and polyphenol content of BPF were determined. Thirty-six female Fisher rats were divided into four groups: control (C); control + BPF (CB); diabetic (D); diabetic + BPF (DB). Diabetes was induced by treatment with streptozotocin. Thirty days after the induction of diabetes, glucose, total cholesterol and triacylglycerides serum levels, aminotransferase and paraoxonase activities were evaluated. Oxidative damage to lipids and proteins was assessed through thiobarbituric acid reactive substances (TBARS) and protein carbonyl analyses, respectively. Histopathological analyses were also performed. BPF contained high concentrations of phenolic compounds, lipids, and fibers, and exhibited a high capacity to neutralize the 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical. Diabetes was evidenced by equivalent high levels of glucose in plasma from rats in the D and DB groups. Diabetic rats in both groups also presented the same increased activity of aminotransferases. Protein carbonyl levels were increased in liver, heart, and pancreas in the D compared with C group. Although treatment with BPF did not result in any histopathological alterations, it reduced significantly the levels of TBARS in the heart and protein carbonyls in the liver and heart. No effect on blood glucose and tissue histology was observed following treatment with BPF. However, BPF diminished oxidative damage in liver and heart, indicating a possible antioxidant potential in vivo, in addition to in vitro(AU)

La harina de pulpa buriti (BPF) contiene niveles significativos de antioxidantes. Este estudio evaluó el efecto del BPF en biomarcadores de daño oxidativo en el hígado, el corazón y el páncreas de ratas diabéticas. Se determino la composición química, la capacidad antioxidante y el contenido de polifenoles del BPF. Treinta y seis ratas Fisher fueron divididas en cuatro grupos: Control (C); Control + BPF (CB); Diabético (D); Diabético + BPF (DB). La diabetes fue inducida por tratamiento con estreptozotocina. Treinta dias después de la inducción de la diabetes, se evaluaron los niveles séricos de glucosa, colesterol total y triacilglicéridos, y las actividades de aminotransferasa y paraoxonasa. El daño oxidativo a lípidos y proteínas se evaluó a través de sustancias reactivas al ácido tiobarbitúrico (TBARS) y análisis de proteínas carboniladas respectivamente. También se realizaron análisis histopatológicos. El BPF contenía altas concentraciones de compuestos fenólicos, lípidos y fibras, y exhibía una alta capacidad para neutralizar el radical 2,2-difenil-1-picrilhidracil (DPPH). La diabetes se evidenció por altos niveles de glucosa en plasma de ratas en los grupos D y DB. Las ratas diabéticas en ambos grupos también presentaron la misma actividad aumentada de las aminotransferasas. Los niveles de proteínas carboniladas se incrementaron en el hígado, el corazón y el páncreas en el grupo D en comparación con el C. Aunque el tratamiento con BPF no dio lugar a alteraciones histopatológicas, redujo significativamente los niveles de TBARS en el corazón y las proteínas carboniladas en el hígado y el corazón. No se observo ningún efecto sobre la glucosa en la sangre y la histología de tejidos después del tratamiento con BPF. Sin embargo, el BPF disminuyó el daño oxidativo en el hígado y el corazón, lo que indica un posible potencial antioxidante in vivo, además de in vitro(AU)

Long-chain ω-6 plasma phospholipid polyunsaturated fatty acids and association with colon adenomas in adult men: a cross-sectional study.

Dietary lipid intake can be associated with an increased risk for colorectal cancer depending on its composition. Carcinogenesis alters lipid metabolism to facilitate cell growth and survival. For instance, metabolites of polyunsaturated fatty acids (PUFAs) are associated with increasing colon cell proliferation. Moreover, precancerous colon lesions (i.e. adenomas) increase the risk for colorectal cancer. In this study, we investigated associations between plasma PUFAs and the number of colon polyps and polyp type (i.e. hyperplastic and adenoma). Healthy male participants (n=126) of 48-65 years of age were recruited before a routine colonoscopy screening. Plasma phospholipid (PPL) PUFAs were isolated by means of solid phase extraction and methylated. Fatty acid methyl esters were analyzed using gas chromatography. Factor analysis was used to cluster PUFAs into groups, and then generated factors and individual PUFAs were analyzed using polytomous logistic regression. In our age-adjusted and smoking-adjusted polytomous logistic regression, for each unit increase in PPL docosatetraenoic acid (DTA), individuals were 1.43 (1.00-2.06) and 1.33 (0.99-1.80) times more likely to have hyperplastic polyps and adenomas rather than no polyps, respectively. In our factor analysis, high PPL ω-6 PUFA and trans-fatty acid loading scores were associated with increased odds of adenoma presence rather than no polyps. Increases in long-chain PPL ω-6 PUFAs are associated with an increased risk for adenomas. As relative levels of DTA increase in PPLs, individuals had increased odds of having hyperplastic polyps and adenomas. Elevated conversion of ω-6 PUFAs to longer-chain ω-6s such as DTA may indicate altered PUFA metabolism at the tissue level.