Preventive effect of Lacticaseibacillus paracasei LMT18-32 on Porphyromonas gingivalis induced periodontitis.

Periodontitis is a severe gum infection leading to chronic inflammation in the gums, damage of tissues around teeth, and destruction of alveolar bones. Porphyromonas gingivalis is the major causative pathogen that induces periodontitis. Numerous probiotic bacteria are reported to produce antibacterial substances against pathogens especially oral pathogens, and these are proposed as preventive measures for periodontitis. In this study, Lacticaseibacillus paracasei LMT18-32 was evaluated and its antibacterial activity against P. gingivalis, and antioxidant activity in vitro were established. In addition, when L. paracasei LMT18-32 was administered to periodontitis induced mice, it successfully alleviated the alveolar bone loss and suppressed induced expression of proinflammatory and tissue destruction related genes in the gingival tissue. In conclusion, L. paracasei LMT18-32 is proposed as a potential probiotics to prevent periodontitis.

Lactobacillus plantarum LMT1-48 exerts anti-obesity effect in high-fat diet-induced obese mice by regulating expression of lipogenic genes.

Obesity is a major health problem and is known to be closely associated with metabolic diseases. Abnormal hepatic accumulation of fat causes fatty liver or hepatic steatosis, and long-term consumption of a high-fat diet is known to be a key obesity-causing factor. Recent studies have demonstrated that probiotics such as Lactobacillus strains, exert an anti-obesity effect by regulating adipogenesis. However, it is still unknown how the consumption of probiotics can reduce abdominal fat volume by regulating the hepatic expression of lipogenic genes. Therefore, we evaluated the effect of long-term ingestion of L. plantarum LMT1-48 on the expression of lipogenic genes in high-fat diet (HFD)-fed mice. We observed that treatment of 3T3-L1 adipocytes with L. plantarum LMT1-48 extract inhibited their differentiation and lipid accumulation by downregulating lipogenic genes, namely, PPARγ, C/EBPα, FAS, and FABP4. Interestingly, administration of L. plantarum LMT1-48 reduced liver weight and liver triglycerides concurrently with the downregulation of the lipogenic genes PPARγ, HSL, SCD-1, and FAT/CD36 in the liver, resulting in the reduction of body weight and fat volume in HFD-fed obese mice. Notably, we also observed that the administration of at least 106 CFU of L. plantarum LMT1-48 significantly lowered body weight and abdominal fat volume in modified diet-fed mouse models. Collectively, these data suggest that L. plantarum LMT1-48 is a potential healthy food for obese people.

Antiobesity Effects of Lactobacillus plantarum LMT1-48 Accompanied by Inhibition of Enterobacter cloacae in the Intestine of Diet-Induced Obese Mice.

The gut microbiota is the most important environmental factor that plays a role in inducing obesity. The gram-negative bacteria, Enterobacter cloacae strains, recently identified in obese mice are considered to be pathogenic bacteria in the gut. Probiotics are important members of the gut microbiota and exert beneficial effects, including inhibiting the growth of potential pathogenic bacteria. Therefore, we isolated a total of 230 lactic acid bacteria from traditional, Korean fermented foods and fecal samples from newborn infants, including Lactobacillus plantarum LMT1-48, which exhibited maximal antimicrobial activity against E. cloacae. We next investigated the functional antiobesity effects of L. plantarum LMT1-48 in an E. cloacae-induced high-fat diet (HFD)-fed animal obesity model. To this end, the L. plantarum LMT1-48 showed antiobesity effects, including body weight loss and reduction of abdominal fat volume, which was accompanied by a decrease in leptin and total cholesterol levels in E. cloacae-induced HFD-fed mice. Notably, gut microbiota diversity also increased after long-term ingestion of L. plantarum LMT1-48, resulting in amelioration of obesity in E. cloacae-induced HFD-fed mice. Accordingly, results suggest that dietary intake of L. plantarum LMT1-48 protects against the onset of E. cloacae-induced obesity.

The Wnt/ß-catenin signaling/Id2 cascade mediates the effects of hypoxia on the hierarchy of colorectal-cancer stem cells.

Hypoxia, a feature common to most solid tumors, is known to regulate many aspects of tumorigenesis. Recently, it was suggested that hypoxia increased the size of the cancer stem-cell (CSC) subpopulations and promoted the acquisition of a CSC-like phenotype. However, candidate hypoxia-regulated mediators specifically relevant to the stemness-related functions of colorectal CSCs have not been examined in detail. In the present study, we showed that hypoxia specifically promoted the self-renewal potential of CSCs. Through various in vitro studies, we found that hypoxia-induced Wnt/ß-catenin signaling increased the occurrence of CSC-like phenotypes and the level of Id2 expression in colorectal-cancer cells. Importantly, the levels of hypoxia-induced CSC-sphere formation and Id2 expression were successfully attenuated by treatment with a Wnt/ß-catenin-signaling inhibitor. We further demonstrated, for the first time, that the degree of hypoxia-induced CSC-sphere formation (CD44(+) subpopulation) in vitro and of tumor metastasis/dissemination in vivo were markedly suppressed by knocking down Id2 expression. Taken together, these data suggested that Wnt/ß-catenin signaling mediated the hypoxia-induced self-renewal potential of colorectal-cancer CSCs through reactivating Id2 expression.