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. 2019 Sep;18(3):1551-1562.
doi: 10.3892/etm.2019.7742. Epub 2019 Jul 5.

Probiotic effect on Helicobacter pylori attachment and inhibition of inflammation in human gastric epithelial cells

Hanyi Song  1 , Long Zhou  2 , Dongyan Liu  3 , Lihui Ge  1 , Yan Li  1
Affiliations

Probiotic effect on Helicobacter pylori attachment and inhibition of inflammation in human gastric epithelial cells

Hanyi Song et al. Exp Ther Med. 2019 Sep.

Abstract

Helicobacter pylori (H. pylori) is a major cause of chronic gastritis, gastric ulcers and gastric cancer. Recent studies have identified that probiotics are beneficial to human health due, in part, to their anti-H. pylori activities. Therefore, the present study investigated the antagonistic and local immunoregulatory activities of seven commercial probiotic strains and explored their mechanisms of actions. The human gastric epithelial cell line-1 (GES-1) was used to assess the effects of probiotics on the adhesion ability of H. pylori. GES-1 cells were infected with H. pylori plus lipopolysaccharide (HP-LPS) or the drug-resistant H. pylori strain (HP021) in the presence or absence of live probiotics. Following this, the growth rate and the adhesion ability of GES-1 cells were detected using MTT and urease activity assay. Toll-like receptor 4 (TLR4), NFKB inhibitor-α (IκBα) and nuclear factor (NF)-κB levels were measured by western blot analysis. The amount of interleukin (IL)-8 in the cell culture medium was determined by ELISA. Amongst the seven probiotic strains studied, live Lactobacillus acidophilus (L. acidophilus) and Lactobacillus bulgaricus (L. bulgaricus) inhibited H. pylori adherence to GES-1 cells most significantly. L. bulgaricus inhibited IL-8 production by GES-1 cells through modulation of the TLR4/IκBα/NF-κB pathway. Therefore, the present results suggested that consumption of food containing L. acidophilus and L. bulgaricus may be used as an adjuvant therapy for H. pylori-associated gastritis.

Keywords: Helicobacter pylori; cell adhesion; inflammation; lipopolysaccharide; probiotics.

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Figures

Figure 1.
Figure 1.
Morphological characteristics of various probiotic strains and H. pylori. (A) Lactobacillus acidophilus, (B) Lactobacillus bulgaricus, (C) Clostridium butyricum, (D) Bifidobacterium longum, (E) Bacillus licheniformis, (F) Lactobacillus salivarius, (G) Bifidobacterium infantis and (H) H. pylori gram staining (red or violet) micrographs under oil immersion (magnification, ×1,000). H. pylori, Helicobacter pylori.
Figure 2.
Figure 2.
Effect of various probiotics strains on GES-1 cell viability. (A) GES-1 cell viability following culture with L. acidophilus, L. bulgaricus, L. 0salivarius, Clostridium butyricum, Bifidobacterium longum, Bifidobacterium infantis or Bacillus licheniformis at a MOI of 100 and (B) MOI of 1,000. (A) *P<0.05 vs. L. acidophilus, L. bulgaricus, L. salivarius, Clostridium butyricum, Bifidobacterium longum, Bifidobacterium infantis; #P<0.05 vs. L. acidophilus, L. bulgaricus, L. salivarius, Clostridium butyricum, Bifidobacterium infantis, Bacillus licheniformis and control group; @P<0.05 vs. L. acidophilus, L. bulgaricus, L. salivarius, Clostridium butyricum, Bifidobacterium infantis, Bifidobacterium longum and control group; &P<0.05 vs. L. acidophilus, L. salivarius, Clostridium butyricum, Bifidobacterium infantis, Bifidobacterium longum, Bacillus licheniformis and control group. (B) *P<0.05 cells vs. L. acidophilus, L. bulgaricus, L. salivarius, Clostridium butyricum, Bifidobacterium longum, Bifidobacterium infantis; #P<0.05 vs. L. acidophilus, L. salivarius, Clostridium butyricum, Bifidobacterium infantis, Bifidobacterium longum, Bacillus licheniformis and control group; @P<0.05 vs. L. acidophilus, L. bulgaricus, L. salivarius, Clostridium butyricum, Bifidobacterium infantis, Bifidobacterium longum and control group; &P<0.05 cells treated with L. bulgaricus, L. acidophilus, L. salivarius, Clostridium butyricum, Bifidobacterium infantis, Bifidobacterium longum vs. Bacillus licheniformis and control group. MOI, multiplicities of infection; L, Lactobacillus.
Figure 2.
Figure 2.
Effect of various probiotics strains on GES-1 cell viability. (A) GES-1 cell viability following culture with L. acidophilus, L. bulgaricus, L. 0salivarius, Clostridium butyricum, Bifidobacterium longum, Bifidobacterium infantis or Bacillus licheniformis at a MOI of 100 and (B) MOI of 1,000. (A) *P<0.05 vs. L. acidophilus, L. bulgaricus, L. salivarius, Clostridium butyricum, Bifidobacterium longum, Bifidobacterium infantis; #P<0.05 vs. L. acidophilus, L. bulgaricus, L. salivarius, Clostridium butyricum, Bifidobacterium infantis, Bacillus licheniformis and control group; @P<0.05 vs. L. acidophilus, L. bulgaricus, L. salivarius, Clostridium butyricum, Bifidobacterium infantis, Bifidobacterium longum and control group; &P<0.05 vs. L. acidophilus, L. salivarius, Clostridium butyricum, Bifidobacterium infantis, Bifidobacterium longum, Bacillus licheniformis and control group. (B) *P<0.05 cells vs. L. acidophilus, L. bulgaricus, L. salivarius, Clostridium butyricum, Bifidobacterium longum, Bifidobacterium infantis; #P<0.05 vs. L. acidophilus, L. salivarius, Clostridium butyricum, Bifidobacterium infantis, Bifidobacterium longum, Bacillus licheniformis and control group; @P<0.05 vs. L. acidophilus, L. bulgaricus, L. salivarius, Clostridium butyricum, Bifidobacterium infantis, Bifidobacterium longum and control group; &P<0.05 cells treated with L. bulgaricus, L. acidophilus, L. salivarius, Clostridium butyricum, Bifidobacterium infantis, Bifidobacterium longum vs. Bacillus licheniformis and control group. MOI, multiplicities of infection; L, Lactobacillus.
Figure 3.
Figure 3.
Binding of various probiotic strains to GES-1 cells. (A) Micrographs demonstrating gram staining of the control group with no probiotics. (B) GES-1 cells cultured with Lactobacillus acidophilus, (C) Lactobacillus bulgaricus, (D) Lactobacillus salivarius, (E) Bifidobacterium longum, (F) Bifidobacterium infantis, (G) Bacillus licheniformis or (H) Clostridium butyricum following Gram staining (red or violet). Green circles highlight probiotics that have adhered to GES-1 cells.
Figure 4.
Figure 4.
Adhesion of various probiotic strains to GES-1 cells. (A) Cell adhesion index of L. acidophilus, L. bulgaricus, L. salivarius, Clostridium butyricum, Bifidobacterium longum, Bifidobacterium infantis and Bacillus licheniformis to GES-1 cells. (B) Cell adhesion rate of L. acidophilus, L. bulgaricus, L. salivarius, Clostridium butyricum, Bifidobacterium longum, Bifidobacterium infantis and Bacillus licheniformis to GES-1 cells. *P<0.05 vs. control group; #P<0.05 vs. L. acidophilus; @P<0.05 vs. Bifidobacterium infantis and Bifidobacterium longum; &P<0.05 vs. Clostridium butyricum and Bacillus licheniformis; αP<0.05 vs. L. bulgaricus. L, Lactobacillus; ns, not significant.
Figure 5.
Figure 5.
Adherence rate of HP to GES-1 cells in the presence of different probiotics at a MOI of 100. (A) Adherence rate of HP to GES-1 cells pretreated with L. acidophilus, L. bulgaricus, L. salivarius, Clostridium butyricum, Bifidobacterium infantis, Bifidobacterium longum, Bacillus licheniformis and CFS of Bacillus licheniformis. (B) Adherence rate of HP to GES-1 cells treated with L. acidophilus, L. bulgaricus, L. salivarius, Clostridium butyricum, Bifidobacterium infantis, Bifidobacterium longum, Bacillus licheniformis and CFS of Bacillus licheniformis following infection (post-treated). *P<0.05 vs. HP group. HP, Helicobacter pylori; L, Lactobacillus; CFS, cell-free supernatant; ns, not significant.
Figure 6.
Figure 6.
Effect of L. acidophilus, L. bulgaricus, L. salivarius, Bifidobacterium infantis, Bifidobacterium longum CFS of Bacillus licheniformis on IL-8 production following HP-LPS treatment. *P<0.05 vs. HP-LPS. HP, Helicobacter pylori; LPS, lipopolysaccharide; IL, interleukin; NS, not significant, L, Lactobacillus.
Figure 7.
Figure 7.
TLR4, IκBα and NF-κB p65 expression by GES-1 cells treated with HP-LPS in the absence or presence of live L. bulgaricus. (A) Representative immunoblots of NF-κB p65 compared with lamin B1 in nuclear extracts. (B) Representative immunoblots of TLR4 and IκBα compared with GAPDH in cytoplasm extracts. (C) Quantification of NF-κB p65, (D) IκBα and (E) TLR4 protein levels following different treatments. *P<0.05 vs. HP-LPS 60 min group; #P<0.05 vs. HP-LPS 120 min group. NF-κB, nuclear factor-κB; TLR4, toll-like receptor 4; IκBα, NFKB inhibitor-α; HP, Helicobacter pylori; LPS, lipopolysaccharide; L, Lactobacillus.
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References

    1. Warren JR, Marshall B. Unidentified curved bacilli on gastric epithelium in active chronic gastritis. Lancet. 1983;1:1273–1275. - PubMed
    1. Kusters JG, van Vliet AH, Kuipers EJ. Pathogenesis of Helicobacter pylori infection. Clin Microbiol Rev. 2006;19:449–490. doi: 10.1128/CMR.00054-05. - DOI - PMC - PubMed
    1. Salama NR, Hartung ML, Müller A. Life in the human stomach: Persistence strategies of the bacterial pathogen Helicobacter pylori. Nat Rev Microbiol. 2013;11:385–399. doi: 10.1038/nrmicro3016. - DOI - PMC - PubMed
    1. Fock KM, Graham DY, Malfertheiner P. Helicobacter pylori research: Historical insights and future directions. Nat Rev Gastroenterol Hepatol. 2013;10:495–500. doi: 10.1038/nrgastro.2013.96. - DOI - PMC - PubMed
    1. Todo K, Ohmae T, Osamura T, Imamura T, Imashuku S. Severe Helicobacter pylori gastritis-related thrombocytopenia and iron deficiency anemia in an adolescent female. Ann Hematol. 2016;95:835–836. doi: 10.1007/s00277-016-2618-x. - DOI - PubMed