CERELA   05438
CENTRO DE REFERENCIA PARA LACTOBACILOS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Immunomodulation by probiotics: Mechanisms envolved
Autor/es:
A. DE MORENO DE LEBLANC
Lugar:
San Miguel de Tucuman, Tucuman, Argentina
Reunión:
Simposio; II Simposio Internacional de Bacterias Lácticas. Primer encuentro Red BAL Argentina.; 2006
Institución organizadora:
CERELA-CONICET
Resumen:
Lactic acid bacteria (LAB) are the most commonly used probiotics. Immune system stimulation is one of the many beneficial effects reported for these bacteria when administered orally. Studies in mice have shown that LAB are able to increase the IgA+ cell number not only in the intestine but also in distant mucosal sites. Viability of the LAB is essential to observe this effect; however, this characteristic is dependent of the bacterial strain. The study of cytokines and cell receptors in lamina propria of the intestine and epithelial cells allows us to suggest the possible mechanisms involved in the modulation of intestinal immunity: LAB or bacterial particles come into contact with epithelial and immune cells thought receptor such as TLR and mannose receptor (CD206). This stimulus activates different immune cells (principally cells from the innate response) that produce an important cytokine profile. This effect was different for each bacterial strain; however, all the probiotic microorganisms maintained the balance between proinflammatory and regulatory cytokines. Cytokine such as IL-10, TGF-b and IL-4 can be implicated in the IgM-IgA switch in B lymphocytes thus allowing IL-6 to promote the clonal expansion of the IgA+ cells increasing the number of this cell population in the lamina propria (principally in the Peyer’ patches). IgA+ cells can also migrate from Peyer’ patches to distant mucosal sites such as in mammary, bronchial tissues and vaginal tissues. We can thus conclude that the innate immune response would be the principal response induced by probiotic microorganisms at the intestinal mucosal level.