Effect of Probiotics Lactobacillus acidophilus and Lacticaseibacillus rhamnosus on Antibacterial Response Gene Transcription of Human Peripheral Monocytes

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Abstract
Periodontitis and related systemic inflammatory diseases are characterized by imbalanced ratio between pro- and anti-inflammatory factors. Probiotics may control inflammation by altering the inflammatory phenotype of defense cells. We aimed to evaluate the gene transcription of the antibacterial response of monocytes to exposure to probiotic lactobacilli. CD14 + monocytes were obtained by positive selection from peripheral blood mononuclear cells from healthy donors (5 × 104 CD14 + /mL) and cultured with probiotic strains of Lacticaseibacillus rhamnosus (LR-32) and Lactobacillus acidophilus (LA-5) at a 1:10 multiplicity of infection in 24-well plates for 12 h. The gene expression analysis was performed by RT-qPCR using the Kit RT2 human antibacterial response, and in the supernatant, the cytokines were determined by ELISA. Tukey’s post hoc test following an ANOVA with a p value of 5% was used for statistical analysis. Both probiotic strains increased the levels of cytokines TNF-α and CXCL-8 in the supernatant compared to the control of non-challenged cells (p < 0.05), but for IL-1Β and IL-6, this effect was observed only for LA-5 (p < 0.05). The fold-regulation values for the following genes for LA-5 and LR-32 were, respectively, IL-12B (431.94 and 33.30), IL-1Β (76.73 and 17.14), TNF-α (94.63 and 2.49), CXCL-8 (89.59 and 4.18), and TLR-2 (49.68 and 3.40). Likewise, most of the other genes evaluated showed greater expression for LA-5 compared to LR-32 (p < 0.05). The positive regulation of inflammatory factors such as IL-1β promoted by L. acidophilus LA-5 may increase the antibacterial activity of innate defense in periodontal tissues. However, this property may be deleterious by increasing inflammatory response.
Funding Information
  • Fundação de Amparo à Pesquisa do Estado de São Paulo (2015/18273-9)
  • Fundação de Amparo à Pesquisa do Estado de São Paulo (2017/10829-3)

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