Anti-inflammatory effects of Lactobacillus brevis K65 on RAW 264.7 cells and in mice with dextran sulphate sodium-induced ulcerative colitis

Abstract

Lactic acid bacteria (LAB) with anti-inflammatory effects may be beneficial to the prevention or treatment for inflammation-related diseases, such as inflammatory bowel diseases. In an in vitro assay, heat-killed Lactobacillus brevis K65 (K65) reduced lipopolysaccharide-induced production of nitric oxide, tumour necrosis factor (TNF)-α and prostaglandin E2 in RAW 264.7 cells. In RAW 264.7 cells stably expressing an ind=ucible nitric oxide synthase (iNOS) reporter, viable K65 showed greater inhibition of iNOS production than its heat-killed form. In order to further examine the in vivo anti-inflammatory effect of K65, viable K65 was orally administered to BALB/c mice before and during the period of dextran sulphate sodium (DSS)-induced ulcerative colitis (UC). K65 improved UC symptoms, including reduced the levels of the pro-inflammatory cytokines, TNF-α, interleukin (IL)-6 and IL-1β, and lowered the activity of myeloperoxidase. Furthermore, K65 inhibited TNF-α, cyclo-oxygenase 2, forkhead box P3, and Toll-like receptor 4 mRNA expression in the colonic tissue of DSS-induced UC mice. Taken together, K65, a LAB with in vitro anti-inflammatory activity showed preventive effects on mice with DSS-induced UC by lowering the expression of inflammatory molecules.

Lactobacillus plantarum L15 Alleviates Colitis by Inhibiting LPS-Mediated NF-κB Activation and Ameliorates DSS-Induced Gut Microbiota Dysbiosis

“…Firstly, the control group was given distilled water, the DDS-induced colitis group (DSS) was received 3.5% (w/v) DSS (36–50 kDa, MP Biomedicals Ltd., Santa Ana, U.S.A.) in drinking water for 7 days. Then, the low-dose (LD) group and the high-dose (HD) group were given 1 × 10 9 or 1 × 10 10 CFU/mL L. plantarum L15 (1 mL/100 g body weight) ( 26 , 27 ) by oral gavage once daily for a period of 28 days, respectively. Bacteria were harvested by centrifugation at 5,000 × g for 10 min.…”

Oral administration of Lactobacillus�plantarum 06CC2 prevents experimental colitis in mice via an anti‑inflammatory response

“…in terms of Lactobacillus members of the Bacilli class, orally administered lP-K68 ameliorated dSS-induced colitis in BalB/c mice by reducing the production of pro-inflammatory cytokines such as TNF-α, il-1β, and il-6 (12). Lactobacillus brevis K65 reduced the levels of the pro-inflammatory cytokines TNF-α, il-6, and il-1β (25). Lactobacillus reuteri F-9-35 prevented dSS-induced colitis by inhibiting the expression of several pro-inflammatory genes, namely those for TnF-α, cyclooxygenase-2, and il-6 (26).…”

“…Lactobacillus and Bifidobacterium, both of which have probiotic characteristics, play a pivotal role in the intestinal environment by preventing pathogen colonization and maintaining normal mucosal immunity. increased numbers of Lactobacillus and Bifidobacterium lead to downregulation of the gene expression of pro-inflammatory cytokines such as TNF-α, il-6, and il-1β (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37)(38)(39)(40)(41). Thus, as a result of changing the composition of the intestinal microflora, heat-killed 06CC2 may indirectly prevent colitis.…”

Lactobacillus plantarum C29 alleviates NF-κB activation and Th17/Treg imbalance in mice with TNBS-induced colitis

“…2015). Studies have reported that Lactobacillus brevis K65 and Lactobacillus paracasei ameliorated DSS-induced ulcerative colitis in mice through the suppression of TNF-α expression (Liu et al, 2016;Pan et al, 2014). Lactobacillus brevis G-101 attenuated colitis by inhibiting TNF-α and IL-1β expression, and by increasing IL-10 expression (Jang et al, 2013).…”