Lactobacilli Reduce Helicobacter pylori Attachment to Host Gastric Epithelial Cells by Inhibiting Adhesion Gene Expression

Abstract

The human gastrointestinal tract, including the harsh environment of the stomach, harbors a large variety of bacteria, of which Lactobacillus species are prominent members. The molecular mechanisms by which species of lactobacilli interfere with pathogen colonization are not fully characterized. In this study, we aimed to study the effect of lactobacillus strains upon the initial attachment of Helicobacter pylori to host cells. Here we report a novel mechanism by which lactobacilli inhibit adherence of the gastric pathogen H. pylori. In a screen with Lactobacillus isolates, we found that only a few could reduce adherence of H. pylori to gastric epithelial cells. Decreased attachment was not due to competition for space or to lactobacillus-mediated killing of the pathogen. Instead, we show that lactobacilli act on H. pylori directly by an effector molecule that is released into the medium. This effector molecule acts on H. pylori by inhibiting expression of the adhesin-encoding gene sabA. Finally, we verified that inhibitory lactobacilli reduced H. pylori colonization in an in vivo model. In conclusion, certain Lactobacillus strains affect pathogen adherence by inhibiting sabA expression and thereby reducing H. pylori binding capacity.

Adhesion and Invasion of Gastric Mucosa Epithelial Cells by Helicobacter pylori

“…However, de Klerk et al (2016) also found certain Lactobacillus strains could inhibit SabA expression at the transcriptional level by releasing an effector molecule into the medium, further affecting H. pylori binding capacity and thereby reducing its adherence. In particular, Lactobacillus , a well-known member of the normal microbiota in the human gastrointestinal tract, has always been studied in relation to H. pylori but largely as a possible supplement for antibiotic treatment (Patel et al, 2014), and interference with H. pylori colonization may contribute to the molecular mechanism for this association (de Klerk et al, 2016). AlpA and AlpB as OMPs also play a role in adherence to host cells and tissues (Odenbreit et al, 1999, 2002a).…”

Helicobacter pylori sabA gene is associated with iron deficiency anemia in childhood and adolescence

“…Many H . pylori characteristics have been related to disease risk, including the cag island encoding both Type IV secretion system and cagA , particular vacA genotypes and genes encoding outer membrane proteins (OMPs), including blood group antigen-binding adhesin BabA, sialic acid-binding adhesin SabA, and outer membrane inflammatory protein OipA [ 3 – 5 ].…”

Helicobacter pylori in ice cream and its control using mastic gum essential oil

“…Majority of these bacteria occur in the mucus layer of the stomach and may act as a reservoir of infection for the underlying gastric epithelium (Dunne et al, 2014). Moreover, it is widely accepted that the bacteria in contact with epithelial cells initiate disease (Klerk et al, 2016). WHO has assorted H. pylori as a class I carcinogen and its elimination with antibiotic combinations has been notified to be profitable in preventing gastric sickness particularly cancer (IARC, 1994) before increasing antibiotic resistance problem which generated an obstacle in treatment of H. pyloriassociated diseases by usual therapies (Murali et al, 2014).…”