The Effect of Lactobacillus acidophilus PTCC 1643 on Cultured Intestinal Epithelial Cells Infected with Salmonella enterica serovar Enteritidis.
10.24171/j.phrp.2017.8.1.07
- Author:
Mona MOSHIRI
1
;
Mohammad Mehdi Soltan DALLAL
;
Farhad REZAEI
;
Masoumeh DOURAGHI
;
Laleh SHARIFI
;
Zahra NOROOZBABAEI
;
Mehrdad GHOLAMI
;
Abbas MIRSHAFIEY
Author Information
1. Division of Microbiology, Department of Pathobiology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. msoltandallal@gmail.com
- Publication Type:Original Article
- Keywords:
Lactobacillus acidophilus;
probiotics;
Salmonella;
gene expression
- MeSH:
Bacteria;
Epithelial Cells*;
Gene Expression;
HT29 Cells;
Humans;
Immunity, Innate;
In Vitro Techniques;
Inflammation;
Lactobacillus acidophilus*;
Lactobacillus*;
Probiotics;
Real-Time Polymerase Chain Reaction;
Salmonella enterica*;
Salmonella enteritidis*;
Salmonella*
- From:
Osong Public Health and Research Perspectives
2017;8(1):54-60
- CountryRepublic of Korea
- Language:English
-
Abstract:
OBJECTIVES: Gastrointestinal disorders caused by Salmonella enterica serovar Enteritidis (SesE) are a significant health problem around the globe. Probiotic bacteria have been shown to have positive effects on the immune responses. Lactobacillus acidophilus was examined for its capability to influence the innate immune response of HT29 intestinal epithelial cells towards SesE. The purpose of this work was to assess the effect of L. acidophilus PTCC 1643 on cultured intestinal epithelial cells infected with SesE. METHODS: HT29 cells were cultured in Roswell Park Memorial Institute medium supplemented with 10% fetal bovine serum and 1% penicillin/streptomycin. The cells were treated with L. acidophilus PTCC 1643 after or before challenge with SesE. At 2 and 4 hours post-infection, we measured changes in the expression levels of TLR2 and TLR4 via real-time polymerase chain reaction. RESULTS: Treatment with L. acidophilus inhibited SesE-induced increases in TLR2 and TLR4 expression in the infected HT29 cells. Moreover, the expression of TLR2 and TLR4 in cells that were pretreated with L. acidophilus and then infected with SesE was significantly higher than that in cells infected with SesE without pretreatment. Taken together, the results indicated that L. acidophilus had an anti-inflammatory effect and modulated the innate immune response to SesE by influencing TLR2 and TLR4 expression. CONCLUSION: Our findings suggested that L. acidophilus PTCC 1643 was able to suppress inflammation caused by SesE infection in HT29 cells and reduce TLR2 and TLR4 expression. Additional in vivo and in vitro studies are required to further elucidate the mechanisms underlying this anti-inflammatory effect.
