CERELA   05438
CENTRO DE REFERENCIA PARA LACTOBACILOS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Lactobacillus jensenii TL2937 regulate the inflammatory response triggered by Toll-like receptor 4 and improve productivity in post-weaning pigs
Autor/es:
JULIO VILLENA; YOSHIHITO SUDA; TAKUYA TAKAHASHI; SEIYA MAKINO; SHUJI IKEGAMI; SUSANA ALVAREZ; HARUKI KITAZAWA
Lugar:
San Miguel de Tucumán, Argentina
Reunión:
Simposio; IV International Symposium on Lactic Acid Bacteria - Food, Health and Applications; 2013
Institución organizadora:
Centro de Referencia para Lactobacilos. CERELA-CONICET
Resumen:
The use of antimicrobials in swine diets tends to be banned to avoid the risk of potential infections with resistant pathogens, resulting in the reduction of productivity. As an alternative, the use of immunoregulatory lactic acid bacteria has been proposed to improve the immune system in piglets in order to avoid intestinal infections and reduce unproductive inflammatory response after weaning. In this regard, we have demonstrated previously that Lactobacillus jensenii TL2937 (LJ) is able to attenuate the inflammatory response triggered by activation of Toll-like receptor 4 (TLR-4) in porcine intestinal epithelial (PIE) cells and antigen presenting cells (APC) from Peyer?s patches (PP). In view of the critical importance of intestinal epithelial cells (IECs)-APCs interactions in the regulation of intestinal immune responses, the aim of the present study was to examine the effect of LJ on activation patterns of APCs from swine PPs in co-cultures with PIE cells. Therefore, we evaluated the functional consequences of indirect exposure of APCs to LJ under non-inflammatory and inflammatory conditions. In addition, this study aimed to investigate whether the previously reported in vitro effects of LJ and extended in this study, were able to beneficially modulate intestinal immunity of piglets after weaning to improve immune-health status. We observed that stimulation of PIE-APCs co-cultures with LJ increased the expression of MHC-II, CD80/86 and IL-10 in CD172a+CD11R1- and CD172a+CD11R1high APC cells (p