Abstract
To evaluate the anti-inflammaging effect of lactic acid bacteria (LAB) on age-dependent inflammation, we first screened and selected a tumor necrosis factor (TNF)-α and reactive oxygen species (ROS)-inhibitory LAB, Lactobacillus pentosus var. plantarum C29, among the LABs isolated from fermented vegetables using LPS-stimulated mouse peritoneal macrophages. Oral administration of C29 (2 × 109 CFU/rat) for 8 weeks in aged Fischer 344 rats (age, 16 months) inhibited the expression of the inflammatory markers myeloperoxidase, inducible nitric oxide (NO) synthase, cyclooxygenase-2, pro-inflammatory cytokines tumor necrosis factor (TNF)-α and IL-6 and the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), activator protein 1 (AP1), and mitogen-activated protein kinases (MAPKs). Treatment with C29 induced the expression of tight junction proteins ZO-1, occludin, and claudin-1, and reduced intestinal microbial LPS and plasmatic LPS levels and ROS, as well as the Firmicutes to Bacteroidetes ratio, which is significantly higher in aged rats than in young rats. C29 treatment also reduced plasmatic reactive oxygen species, malondialdehyde, C-reactive protein, and TNF-α, and suppressed expression of senescence markers p16 and p53 in the colon of the aged rats, but increased SIRT 1 expression. Based on these findings, we concluded that C29 treatment may suppress aging-dependent colitis by inhibiting NF-κB, AP1, and MAPK activation via the inhibition of gut microbiota LPS production and the induction of tight junction protein expression.
Highlights
Aging is an inevitable consequence of processes characterized by age-dependent physiological and functional decline and is hypothesized to be closely associated with chronic inflammatory states [1,2]
To evaluate the effect of anti-inflammatory lactic acid bacteria (LAB) on age-dependent inflammation, we screened tumor necrosis factor (TNF)-α expression-inhibitory LAB from collected kimchi LAB strains in LPS-stimulated rat peritoneal macrophages
Hopkins et al found that Bifidobacterium and Lactobacillus levels were lower in elderly people than in younger adults, whereas Bacteroides and Eubacterium levels were the same [32]
Summary
Aging is an inevitable consequence of processes characterized by age-dependent physiological and functional decline and is hypothesized to be closely associated with chronic inflammatory states [1,2]. Oxidative stress continuously activates low-grade inflammatory signaling pathways via the redox-sensitive nuclear factor-kappa B (NF-κB) signaling pathway [1,3], leading to the chronic inflammatory diseases colitis and rheumatoid arthritis, and the age-related degenerative diseases Alzheimer’s disease [4,5,6,7] and cardiovascular disease [8]. LPS significantly stimulates an inflammatory response via the CD14/TLR4/MD2 receptor complex in many cell types, such as monocytes, dendritic cells, macrophages and B cells. LPS stimulation can induce reactive oxygen species (ROS) production via nicotinamide adenine dinucleotide phosphate oxidase activation in immune cells such as neutrophils. Little is known about the molecular mechanism underlying gut microbiota LPS-stimulated aging
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