Submitted to: Journal of Animal Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: October 12, 2010
Publication Date: January 1, 2011
Citation: Kerr, B.J., Weber, T.E., Ziemer, C.J., Spence, C., Cotta, M.A., Whitehead, T.R. 2011. Effect of dietary inorganic sulfur level on growth performance, fecal composition, and measures of inflammation and sulfate-reducing bacteria in the intestine of growing pigs. Journal of Animal Science. 89:426-437. Interpretive Summary: Investigation of sulfur (S) metabolism in swine has typically focused on sulfur amino acid nutrition, with little attention on levels of inorgainc sulfur. However, because various corn co-products can have elevated levels of total sulfur and because intestinal hydrogen sulfide levels may affect gastrointestinal health and function, more information is needed on the impact of inorganic S on pig performance, intestinal inflammation, and manure composition. The data suggest that growing pigs can tolerate relatively high levels of dietary inorganic S, well above the levels that would be found by feeding high levels of corn co-products, but exceedingly high dietary S levels can alter inflammatory mediators in the intestine and intestinal bacteria populations. This information is important for nutritionists at universities, feed companies, and swine production facilities showing that the levels of sulfur contained in corn co-products would not impact pig performance and intestinal health, but very high levels of inorganic sulfur (either from feedstuffs or water) may affect pig performance and gastrointestinal function.
Technical Abstract: Two experiments were conducted to investigate the impact of dietary inorganic S on growth performance, markers of intestinal inflammation, fecal composition, and the presence of sulfate-reducing bacteria (SRB). In Exp. 1, pigs (n = 42; 13.8 kg) were fed diets formulated to contain either 2,300 or 2,100 ppm S for 24 d. Lowering dietary S had no effect on ADG, ADFI, or G:F. In Exp. 2, pigs (n = 64; 13.3 kg) were fed diets containing 0, 0.625, 1.25, 2.5, or 5.0% CaSO4, thereby increasing dietary S from 2,900 to 12,100 ppm. Two additional diets were fed to confirm the lack of an impact due to feeding 'low' dietary S on pig performance and to determine if the elevated Ca and P levels in the diets containing CaSO4 had an impact on growth performance. Pigs were fed for 35 d. Ileal tissue, ileal mucosa, and colon tissue were harvested from pigs fed the 0 and 5% CaSO4 diets (Low-S and High-S, respectively) to determine the impact of dietary S on inflammation-related mRNAs, activity of mucosal alkaline phosphatase and sucrase; and pathways of inflammatory activation. Real-time PCR was used to quantify SRB in ileal and colon digesta samples and feces. Fecal pH, sulfide, and ammonia levels were also determined. There was no impact on growth performance in pigs fed the diet reduced in dietary S or by the elevation of dietary Ca and P. Increasing dietary S from 2,900 to 12,100 ppm had a linear (P < 0.01) effect on ADG and a cubic effect (P < 0.05) on ADFI and G:F. Real-time RT-PCR analysis revealed that pigs fed High-S increased (P < 0.05) the relative abundance of intracellular adhesion molecule-1, tumor necrosis factor-a, and suppressor of cytokine signaling-3 mRNA, and tended (P < 0.09) to increase the relative abundance of IL-6 mRNA in ileal tissue. Likewise, pigs fed High-S had reduced (P < 0.05) levels of nuclear factor of light polypeptide gene enhancer in B-cells inhibitor-a and increased (P < 0.05) phospho-p44/p42 mitogen activated protein kinase in ileal tissue, but there was no effect of dietary S on mucosal alkaline phosphatase or sucrase activity. Pigs fed the High-S diet had decreased (P < 0.05) total bacteria levels in ileal digesta, but increased (P < 0.05) prevalance of SRB in colon contents. Fecal sulfide was increased (P < 0.05) and fecal pH was deceased (P < 0.05) in pigs fed High-S. The data suggest that growing pigs can tolerate relatively high levels of dietary inorganic S, but high dietary S levels alter inflammatory mediators and levels of intestinal bacteria.