Butyrate modulates mucin secretion and bacterial adherence in LoVo cells via MAPK signaling.
Tae-Hwan JungKyoung-Sik HanJeong-Hyeon ParkHyo-Jeong HwangPublished in: PloS one (2022)
Short-chain fatty acids contribute to normal bowel function and prevent bacterial infections. In particular, butyrate is a promising candidate that plays an important role in regulating the functional integrity of the gastrointestinal tract by stimulating mucin secretion. We investigated whether butyrate treatment modulates mucin secretion and bacterial adherence in LoVo cells. In addition, the possible signaling pathways were also examined in connection with the upregulation of mucin secretion. The results showed that butyrate induced mucin secretion in LoVo cells, resulting in the inhibition of Escherichia coli adhesion by increasing the adherence of Lactobacillus acidophilus and Bifidobacterium longum. The gene expression analysis suggests that mitogen-activated protein kinase (MAPK) signaling pathways including Cdc42-PAK pathway appears to be involved in stimulating mucin secretion. More importantly, butyrate induced the increased actin expression and polymerization in LoVo cells, which could be attributable to the Cdc42-PAK signaling pathway, implicated in actin cytoskeleton and mucin secretion. Our results provide a molecular basis in modulating bacterial adherence and the MAPK signaling pathway for the improved homeostasis of colonic epithelial cells.
Keyphrases
- signaling pathway
- induced apoptosis
- pi k akt
- cell cycle arrest
- epithelial mesenchymal transition
- escherichia coli
- oxidative stress
- endoplasmic reticulum stress
- cell proliferation
- type diabetes
- high glucose
- adipose tissue
- cell death
- metabolic syndrome
- endothelial cells
- staphylococcus aureus
- multidrug resistant
- mass spectrometry
- glycemic control
- ulcerative colitis
- copy number
- drug induced
- pseudomonas aeruginosa
- candida albicans
- binding protein
- smoking cessation
- weight loss
- tyrosine kinase
- insulin resistance