<sec><title>Objectives</title><p>Gastrointestinal disorders caused by <italic>Salmonella enterica</italic> serovar Enteritidis (<italic>Se</italic>sE) are a significant health problem around the globe. Probiotic bacteria have been shown to have positive effects on the immune responses. <italic>Lactobacillus acidophilus</italic> was examined for its capability to influence the innate immune response of HT29 intestinal epithelial cells towards <italic>Se</italic>sE. The purpose of this work was to assess the effect of <italic>L. acidophilus</italic> PTCC 1643 on cultured intestinal epithelial cells infected with <italic>Se</italic>sE.</p></sec><sec><title>Methods</title><p>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 <italic>L. acidophilus</italic> PTCC 1643 after or before challenge with <italic>Se</italic>sE. At 2 and 4 hours post-infection, we measured changes in the expression levels of <italic>TLR2</italic> and <italic>TLR4</italic> via real-time polymerase chain reaction.</p></sec><sec><title>Results</title><p>Treatment with <italic>L. acidophilus</italic> inhibited <italic>Se</italic>sE-induced increases in <italic>TLR2</italic> and <italic>TLR4</italic> expression in the infected HT29 cells. Moreover, the expression of <italic>TLR2</italic> and <italic>TLR4</italic> in cells that were pretreated with <italic>L. acidophilus</italic> and then infected with <italic>Se</italic>sE was significantly higher than that in cells infected with <italic>Se</italic>sE without pretreatment. Taken together, the results indicated that <italic>L. acidophilus</italic> had an anti-inflammatory effect and modulated the innate immune response to <italic>Se</italic>sE by influencing <italic>TLR2</italic> and <italic>TLR4</italic> expression.</p></sec><sec><title>Conclusion</title><p>Our findings suggested that <italic>L. acidophilus</italic> PTCC 1643 was able to suppress inflammation caused by <italic>Se</italic>sE infection in HT29 cells and reduce <italic>TLR2</italic> and <italic>TLR4</italic> expression. Additional in vivo and in vitro studies are required to further elucidate the mechanisms underlying this anti-inflammatory effect.</p></sec>
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