Lactobacillus paracasei strain 06TCa19 suppresses inflammatory chemokine induced by Helicobacter pylori in human gastric epithelial cells

Abstract

Helicobacter (H.) pylori infection is an important risk factor for gastric cancer that causes gastric inflammation. Inflammatory chemokines such as interleukin (IL)-8 and regulated on activation normal T cell expressed and secreted (RANTES) are elevated in the gastric mucosa by H. pylori. This study aimed to investigate the effects of Lactobacillus paracasei strain 06TCa19, a probiotic strain, on IL-8 and RANTES expression and production induced by H. pylori using human gastric epithelial cell lines. Strain 06TCa19 was shown to suppress H. pylori-mediated elevation of gene expression related to these chemokines in MKN45 cells. The strain also suppressed the increase in IL-8 and RANTES products induced by H. pylori in AGS cells as well as in MKN45 cells. In MKN45 cells inoculated with H. pylori, strain 06TCa19 was shown to downregulate the activation of NF-κB and p38 MAPK signaling pathways. Additionally, the level of the CagA virulence protein of H. pylori in the MKN45 cells and the number of viable H. pylori adhering to MKN45 cells decreased with the addition of strain 06TCa19. Moreover, the strain 06TCa19 notably increased lactic acid in the supernatant of MKN45 cells. Thus, lactic acid released from strain 06TCa19 might have inhibited the adhesion of H. pylori to MKN45 cells and prevented the insertion of H. pylori CagA into the cells, and elevation of IL-8 and RANTES genes and proteins might be suppressed by downregulating the NF-κB and p38 MAPK pathways. Therefore, use of strain 06TCa19 may prevent H. pylori-associated gastric inflammation.

Probiotics alter the immune response of gingival epithelial cells challenged by Porphyromonas gingivalis

“…This activity of probiotics may not only affect P. gingivalis colonization levels, but may also prevent the mechanisms by which this keystone pathogen favors the growth of the entire microbial community and leads to dysbiosis by promoting a localized chemokine paralysis . A recent study revealed that co‐culture of L. paracasei and human gastric epithelial cell lines infected with H. pylori resulted in decreased adhesion and reduced CXCL8 expression, which is elevated in the gastric mucosa by Helicobacter pylory . This difference clearly illustrates that probiotics modulatory properties should be explored according to the imbalance in innate response induced by specific pathogens on mucosa surfaces.…”

Antibacterial Activity of Lactic Acid Bacteria against Helicobacter pylori Evidence by in vivo and in vitro Studies

“…Cats et al, (2003) found that culture and supernatants from L. casei grown in MRS medium significantly induced clear inhibition zone of H. pylori. Also, another study found that use of L. paracasei strain 06TCa19 may prevent H. pylori associated gastric inflammation (Takeda et al, 2017).…”

Fermented milk containing Lactobacillus paracasei and Glycyrrhiza glabra has a beneficial effect in patients with Helicobacter pylori infection

“…[13,61] Most effective strain of probiotics has not been determined yet for the management of H pylori infection, but Lactobacillus species showed proven efficacy because they are resistant to acidic environment, pancreatic enzyme, and bile salts and release lactic acid inhibiting the adhesion of H pylori to the cells. [43,62–64] In our study, L paracasei was used because it can produce a remarkable amount of lactic acid, which is regarded as the origin of anti- H pylori activity, [65] and has better immunomodulatory function in preventing intestinal inflammation than L plantarum or L rhamnosus . [16,66] Furthermore, L paracasei inhibited the elevation of IL-8 and regulated upon activation, normal T-cell expressed and presumably secreted (RANTES) released from the H pylori -infected gastric epithelium.…”

“…[16,66] Furthermore, L paracasei inhibited the elevation of IL-8 and regulated upon activation, normal T-cell expressed and presumably secreted (RANTES) released from the H pylori -infected gastric epithelium. [62,67]…”