Kefir modulates gut microbiota and reduces DMH-associated colorectal cancer via regulation of intestinal inflammation in adulthood offsprings programmed by neonatal overfeeding.

Obesity is associated with chronic inflammation, intestinal dysbiosis, and colorectal cancer risk. The anti-cancer effects of kefir are highlighted. Here, lactating Wistar rats were divided into: Normal litter (NL); Kefir normal litter (KNL); Small litter (SL); Kefir small litter (KSL). The NL and SL groups received 1 mL of water/day; KNL and KSL received kefir milk daily (108 CFU/mL) during lactation. After weaning, the pups continued to receive the same treatments until 60 days. At 67 days old, colorectal carcinogenesis was induced through intraperitoneal injection of 1,2-dimethylhydrazine. At 240 days, visceral adipose tissue was higher in SL compared to NL, KNL, and KSL. Kefir intake was found to suppress the number of tumors in both KNL and KSL groups (-100% and -71.43%; p < 0.01, respectively). IL-1ß, IL-6, TNF-α, and NO levels in the colon were higher in the NL and SL compared to the KNL and KSL. The gut microbiota in cecal samples of SL was enriched with Alloprevotella, Acinetobacter, and Bacteroides. In contrast, the cecal contents of KSL and KNL were higher Romboutsia. Thus, neonatal overfeeding leads to greater adiposity, inflammation and number of colon tumors in adulthood. Early-life nutrition based on kefir reverted these alterations.

Parthenolide Modulates Immune Response in Cells from C57BL/6 Mice Induced with Experimental Autoimmune Encephalomyelitis.

Multiple sclerosis is a chronic inflammatory and autoimmune disease of the central nervous system that affects more than 2.5 million people worldwide. Experimental autoimmune encephalomyelitis is a murine autoimmune disease used to study multiple sclerosis. Parthenolide, a natural sesquiterpene lactone found in Tanacetum parthenium L., is known for its strong anti-inflammatory activity. Herein, we have investigated the in vitro immunomodulatory effects of parthenolide on cytokine production and nitric oxide in cultured cells from myelin oligodendrocyte glycoprotein 35-55 amino acid peptide mice. Experimental autoimmune encephalomyelitis was induced in C57BL/6 mice with myelin oligodendrocyte glycoprotein 35-55 amino acid peptide, and parthenolide was isolated from T. parthenium. Splenocytes and peritoneal cells were obtained from experimental autoimmune encephalomyelitis-induced mice and incubated with parthenolide (1, 5, and 20 µM). After in vitro treatment with parthenolide, supernatants were collected, and nitric oxide and cytokines were measured. The results suggested that parthenolide may regulate the activity of Th17 and Th1 cells, mainly by decreasing IL-17, TNF-α, and interferon gamma production. This modulation may be related to the lower levels of IL-12p40 and IL-6 after treatment with parthenolide. It was shown, for the first time, that parthenolide presents in vitro immunomodulatory effects on inflammatory mediators produced by cells from experimental autoimmune encephalomyelitis-induced mice.