The nonantibiotic anti-inflammatory effect of antimicrobial growth promoters, the real mode of action? A hypothesis.

Societal concern and government regulations increasingly press for restricting the use of antibiotics as antimicrobial growth promoters (AGP). The search for alternatives is on, hampered by a lack of knowledge about the exact mechanism of AGP. Feed additives, such as AGP and alternatives, interact with the intestine. In the intestine, feed components, microbiota, and the mucosa interact in a very complex and dynamic way. Various mechanisms for AGP have been proposed, invariably based on the direct antibiotic influence on the microbial composition of the intestines. In the literature on antibiotics, however, the direct effects of antibiotics on host cells, in particular inflammatory cells, have been described. It is curious that this has never been considered in the literature on AGP. Presently, a case is being made that AGP most likely work as growth permitters by inhibiting the production and excretion of catabolic mediators by intestinal inflammatory cells. Concomitant or subsequent changes in microflora are most likely the consequence of an altered condition of the intestinal wall. This common, basic mechanism potentially offers an excellent explanation for the highly reproducible effects of AGP, as opposed to those obtained by alternatives aimed at microflora management. Therefore, the search for alternatives could be aimed at nonantibiotic compounds with an effect on the inflammatory system similar to that of AGP.