According to Salmon, the survival of neonate piglets depends directly on the acquisition of maternal immunity via colostrum then milk, affording respectively systemic and mucosal protection. Yeast has long been known to help intestinal flora recovery after pathogen challenges. The speaker said that concerning yeast, SC boulardii had been first described to decrease diarrhea occurrence in consumers of litchis in Cambodia at the beginning of the 20th century.
The immunity system is compartmentalized: the IgM molecules are very heavy and don’t move fast enough to fight disease, so IgG is the queen of the fight in all the cellules spaces, with an adhesive action on the pathogen (antiseptic immunity) and IgA is a kind of “fly killer paper” as it is placed on the mucus. The pathogen adheres to IgA and, with intestinal peristaltic, is excreted with mucus. Thus, the piglet immunity system uses two different strategies to reduce the occurrence of diarrhea. Before farrowing, the sow concentrates IgG. Through the colostrum, she gives a kind of “bolus” of IgG to the piglets that can be used during the first 36 hours, as the digestive tract is very permeable. Then milk contributes for IgA. Whereas colostral IgG are mainly due to accumulation of blood IgG in the acini of the mammary gland at the end of the pregnancy, milk IgA originates from plasma cells: according to their homing receptors, these cells originate from separate mucosal compartments in the respiratory tract and intestine. Such entero-mammary links may be induced or enhanced by probiotic in the feed. The scientist investigates if feeding some sows with various S cerevisiae strains may increase the IgA in colostrum or/and in milk.
Feeding pregnant sows with S cerevisiae strain CNCM I 3856 at 0.05% increases concentration of IgG in colostrum and IgA in milk. It also 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 the milk might be due to persistence of plasma cells in mammary gland and/or in gut and/or lower decay of plgR (translocation site).
Acidity in the intestinal tractus also influences the IgA: it has been shown that butyrate, for example, is able to activate the transport system of IgA, which, in turn, is an incitation to increase the IgA production. Any action improving the IgA production in the sow has a protective action through the milk in the piglet.
In vitro study had been realized at the same time with the same yeast strain. It modulates epithelial cell responses to F4+ E.coli (ETEC) by decreasing the expression of pro-inflammatory transcripts. At the same time, there was a decrease in the mitogen-activated protein kinases ERK ½ and p38 phosphorylation. S. Cerevisiae regulates mRNA levels of the anti-inflammatory PPAR-gamma nuclear receptor, the IL-12p35 cytokine and the CCL25 chemokine involved in gut mucosal immunity.
Salmon concluded that S. cerevisiae strain CNCM I 3856 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.