ISSUE FOCUS 50 FEED & ADDITIVE MAGAZINE April 2023 of SINS. This is because endotoxins can trigger the release of pro-inflammatory mediators and cause a systemic inflammatory response leading to multiple organ failure. It should be noted that the relationship between SINS and endotoxins is not fully understood yet and more research is needed to understand and confirm the exact mechanism. SIMILAR MODES OF ACTION It is believed that SINS is caused by a systemic inflammatory response, which is characterized by the release of pro-inflammatory mediators such as cytokines. Cytokines are a group of small proteins that are involved in the regulation of the immune response. Some of the pro-inflammatory cytokines that have been associated with SINS include tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6). All of these potent pro-inflammatory cytokines are involved in the regulation of the immune response and are known to play roles in the development of inflammation and tissue damage associated with various diseases. Since endotoxins trigger a proinflammatory reaction mediated through some of the same cytokines associated with SINS, it seems to confirm the hypothesis that endotoxins are one of the factors involved in SINS. Since there is evidence of the association of SINS with the presence of endotoxins, reducing the impact of endotoxins in pigs may contribute to reducing the incidence and virulence of SINS. Studies performed at the University of Ghent have demonstrated the capacity of some toxin binders to capture endotoxins in the gastrointestinal tract, thus stopping their action in the intestinal epithelium and limiting adsorption to the bloodstream. The study demonstrated the effect of the toxin binder in reducing the production of inflammatory cytokines. Precisely the same mediators associated with SINS as described before. In the study, the authors compared the effect on the production of cytokines by injection of endotoxins with or without the addition of the toxin binder. Based on a model of Vandenbroucke et al., 2011, the ex vivo model was intestinal loops of live piglets. The study consisted of surgery on two female piglets at 5 weeks of age. Intestinal loops 8 cm long of jejunum were used as experimental units (Figure 2). SET-UP OF THE TOXIN BINDER TRIAL AGAINST ENDOTOXINS The data from this trial (Figures 3 & 4) proved that the toxin binder was capable of reducing cyFigure 2. In two 5-week-old piglets, 3 intestinal loops per treatment of 8 cm were produced at the level of the jejunum. Different conditions were then injected directly in the intestinal loop and a biopt of each look was taken to determine endotoxin binding potential
RkJQdWJsaXNoZXIy MTUxNjkxNQ==