Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 3/15/2013
Publication Date: 4/24/2013
Citation: Genovese, K.J., Harvey, R.B., He, L.H., Nisbet, D.J. 2013. Systemic response to host microflora in gnotobiotic pigs. The Gut Microbiota: The Effector/Regulatory Immune Network. February 10-15, Taos, NM. p. 52(1030).
Technical Abstract: The importance of the development and maintenance of a healthy gut microflora from birth throughout life has become a major focus. To this end, our laboratory has developed a porcine-derived mixed bacterial culture (CF) isolated from the ceca of a healthy, pathogen-free pigs. The CF culture has been shown to protect neonatal and weaned pigs from infection and disease caused by food-borne pathogens such as Salmonella and disease-causing bacteria such as E. coli. The mechanism of action of the protection from pathogens observed with the CF culture remains unclear; however, recent evidence suggests that the initial interactions between the host and its microflora soon after birth may aid in the development of the immune system of neonates and in “tolerance” or acceptance of the host’s microflora. In the present study, piglets from four sows were delivered by caesarian section and reared under gnotobiotic conditions. Piglets were either given CF within 1 hr after birth or were given sterile media. At times 0, 8, 24, 48, and 72 hours post-birth, piglets were euthanized and splenic samples were taken. Splenic cells from individual piglets were isolated and cultured with or without concanavalin A (conA). Splenic cells from CF-treated piglets had increased production of IL-1ß, IFN-gamma, IL-18, and IL-10 at 8 hours after birth compared to control piglets as measured by porcine cytokine ELISA. The increased levels of cytokines produced by CF-treated piglet splenocytes then declined over time, returning to levels observed in control pigs or in some instances, below control levels. These results suggest that CF may act as a modulator for certain aspects of systemic innate immune development.