Probiotic Lactic Acid Bacteria, Ochratoxin A, And Immunomodulation

RODRIGUEZ AV

Mendoza, Argentina

Simposio; MyCo Red Argentina. ISM Conference 201; 2011

Probiotic Lactic Acid Bacteria, Ochratoxin A, And Immunomodulation Ana V. RODRIGUEZ Centro de Referencia para Lactobacilos- CERELA-CONICET. Tucumán, Argentina.e-mail: anavirr@cerela.org.ar Lactobacilli are one of most relevant beneficial organisms termed probiotics, defined as “live microorganisms which when administered in adequate amounts confer health benefits to the host”. Today, a large number of commercial products including fermented foods and food complements contain probiotics because of their role as modulator of pro- and anti-inflammatory cytokines. Our laboratory is studying target cell-probiotic interaction using human peripheral blood mononuclear cells (PBMC) as a model system, and the molecular mechanism involved in cell response. Particularly, we investigate the participation of membrane microdomains of PBMS, named membrane rafts, in the immune response modulated by lactobacilli. Our work indicate that two probiotic LAB, Lactobacillus reuteri CRL 1098 (Lr) and Lactobacillus acidophilus CRL 1014 (La), modulate the immune response in different way: Lr dimishes TNF-α and apoptosis, while no effect is observed on IL-10. La increases TNF-α, IL-10 and apoptosis in PBMC. When PBMC membrane rafts were disrupted by extraction of chlolesterol, these cellular responses induced by both, La and Lr, were increased, indicating a potential role of rafts in bacteria-cell interaction. Further studies demonstrate that reduced TNF-α production induced by Lr involves the mobilization of marker protein Lck from membrane rafts. Using the model of PBMC, we investigate whether Lr and La modify the ochratoxin A (OTA) effects on TNF-α, IL-10 production and apoptosis. The toxin diminishes TNF-α and IL-10, and strongly increased the apoptotic cells. Both, Lr and La, diminish TNF-α inhibition produced by the toxin, while no effect is observed in IL-10 level. Lr and La protect PBMC from OTA-induced apoptosis, as measured by the reduction of apoptotic cells from 20% to 14%. OTA induced apoptosis to a lower extent in control cells than in disrupted-rafts cells, indicating that membrane rafts may also play a role in this response. Our data show that Lr and La diminish OTA induced-apoptosis PBMC and disrupted-rafts PBMC, even when recent findings from our laboratory reveal that Lr is anti-apoptotic and La is pro-apoptotic. These data suggest that each bacterium could trigger different pathways for reverting apoptosis induced by OTA. Our results provide evidences that support the role of LAB for restricting some immune-toxic effects of OTA. They also highlight the potential participation of membrane rafts in molecular mechanisms involved in reduction of OTA immunotoxicity by LAB.