Anti-bacterial effects of enzymatically-isolated sialic acid from glycomacropeptide in a Helicobacter pylori-infected murine model.
- Author:
Hye Ji NOH
1
;
Hong Bum KOH
;
Hee Kyoung KIM
;
Hyang Hyun CHO
;
Jeongmin LEE
Author Information
- Publication Type:Original Article
- Keywords: Sialic acid; Helicobacter pylori; cytotoxin-associated gene A
- MeSH: Animals; Anti-Bacterial Agents; Body Weight; Coculture Techniques; Colon; Cytokines; Duodenum; Enzyme-Linked Immunosorbent Assay; Helicobacter pylori; Helicobacter*; Humans; In Vitro Techniques; Interleukin-10; Interleukin-6; Interleukin-8; Methods; Mice; Mucous Membrane; N-Acetylneuraminic Acid*; Necrosis; Pathology; Real-Time Polymerase Chain Reaction; Stomach; Stomach Diseases; Whey
- From:Nutrition Research and Practice 2017;11(1):11-16
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND/OBJECTIVES: Helicobacter pylori (H. pylori) colonization of the stomach mucosa and duodenum is the major cause of acute and chronic gastroduodenal pathology in humans. Efforts to find effective anti-bacterial strategies against H. pylori for the non-antibiotic control of H. pylori infection are urgently required. In this study, we used whey to prepare glycomacropeptide (GMP), from which sialic acid (G-SA) was enzymatically isolated. We investigated the anti-bacterial effects of G-SA against H. pylori in vitro and in an H. pylori-infected murine model. MATERIALS/METHODS: The anti-bacterial activity of G-SA was measured in vitro using the macrodilution method, and interleukin-8 (IL-8) production was measured in H. pylori and AGS cell co-cultures by ELISA. For in vivo study, G-SA 5 g/kg body weight (bw)/day and H. pylori were administered to mice three times over one week. After one week, G-SA 5 g/kg bw/day alone was administered every day for one week. Tumor necrosis factor-α (TNF-α), IL-1β, IL-6, and IL-10 levels were measured by ELISA to determine the anti-inflammatory effects of G-SA. In addition, real-time PCR was performed to measure the genetic expression of cytotoxin-associated gene A (cagA). RESULTS: G-SA inhibited the growth of H. pylori and suppressed IL-8 production in H. pylori and in AGS cell co-cultures in vitro. In the in vivo assay, administration of G-SA reduced levels of IL-1β and IL-6 pro-inflammatory cytokines whereas IL-10 level increased. Also, G-SA suppressed the expression of cagA in the stomach of H. pylori-infected mice. CONCLUSION: G-SA possesses anti-H. pylori activity as well as an anti-H. pylori-induced gastric inflammatory effect in an experimental H. pylori-infected murine model. G-SA has potential as an alternative to antibiotics for the prevention of H. pylori infection and H. pylori-induced gastric disease prevention.
