The survival of neonate piglets depends directly on the acquisition of maternal immunity via colostrum, and milk affording systemic and mucosal protection, respectively. Whereas colostral IgG are mainly due to accumulation of blood IgG in the acini of the mammary gland at the end of pregnancy, milk IgA originates from plasma cells; according to their homing receptors these cells orginate form separate mucosal compartments in the respiratory tract and intestine. Such immune entero-mammary link may be induced or enhanced by probiotic in the feed. Thus we asked if feeding sows with various S. cerevisiae strains may increase the IgA in colostrum and /or milk.
Feeding pregnant sows with S. cerevisiae strain CNCM I-3856 (Actisaf Sc 47) at 0.05% increases concentrations of IgG in colostrum and IgA in milk and decreases the incidence of non-typed E. coli diarrhea in piglets. Higher IgG concentration in the colostrum may be associated with increase of blood IgG translocation (more FcRn) and maintenance of IgA level in milk may be due i) to persistence of plasma cells in mammary gland and/or in gut ii) and/or lower decay of pIgR.
At the same time, in in vitro studies, with S. cerevisiae strain CNCM I-3856 (Actisaf Sc 47) modulates epithelial cell responses to F4+ E. coli by decreasing the expression of pro-inflammatory transcripts (TNF-α, IL-1α, IL-6, IL-8, CXCL2 and CCL20). Concomitantly, there was a decrease in the mitogen-activated protein kinases ERK1/2 and p38 phosphorylation. In contrast, S. cerevisiae up-regulates mRNA levels of the anti-inflammatory PPAR-γ nuclear receptor, the IL-12p35 cytokine and the CCL25 chemokine involved in gut mucosal immunity.
Thus with S. cerevisiae strain CNCM I-3856 (Actisaf Sc 47) exhibits various probiotic properties enhancing the sow-mediated immunity probably by intervening at several complementary levels, the resident microflora of the gut and the gut epithelial cells.
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