The tissue injury at the early stages of the heat stress response triggers release of inflammatory and oxidative agents from intestinal content into the milieu of the body. Intestinal homeostasis (i.e., eubiosis) improves the barrier function and mitigates the gut-derived influx of endotoxins. In this study we have analyzed the mitigating role of embryonic stimulation of the gut homeostasis in chickens on immune and oxidative responses to heat. The animal trial was conducted on broiler chickens. The treatment included a single in ovo injection of the galactooligosaccharides (GOS) prebiotic into the air cell of the egg on day 12 of incubation. Control eggs were in ovo injected with the same volume of sterile physiological saline. After hatching, birds were raised in group pens (6 pens/group, 25 birds/pen). Short-term, mild heat stress was induced on day 32 post-hatching by increase in the ambient temperature above the thermal comfort (30 °C for 8.5 h). The spleen was harvested from randomly selected individuals. The relative gene expression study was conducted with RT-qPCR. The two gene panels were analyzed: (1) immune response genes (IL-1β IL-2, IL-4, IL-6, IL-12p40 and IL-17) and (2) stress response genes (HSP25, HSP70, HSP90, BAG3, CAT and SOD). Data were evaluated by the analysis of variance in a 2 × 2 factorial design that included in ovo treatment and ambient temperature as factors. We have found that the immune-related and stress-related gene expression signatures were triggered in animals subjected to heat but with unbalanced intestinal flora (i.e., dysbiotic, without in ovo stimulation with GOS). These animals had increased expression of the genes involved in the immune responses (IL-4 and IL17) and stress responses (HSP25, HSP70, HSP90, CAT and SOD) to short-term heat stress that indicated presence of inflammatory and oxidative mediators (P < 0.05). The individuals that were in ovo stimulated with GOS did not mount the anti-inflammatory or antioxidative responses. Heat shock proteins (HSP25 and HSP70) were increased in both groups challenged with heat, which indicated their role in adaptation to heat.
A. Slawinska, S. Mendes, A. Dunislawska, M. Siwek, M. Zampiga, F. Sirri, et al. (2019). Avian model to mitigate gut-derived immune response and oxidative stress during heat. BIOSYSTEMS, 178, 10-15 [10.1016/j.biosystems.2019.01.007].
Avian model to mitigate gut-derived immune response and oxidative stress during heat
M. Zampiga;F. Sirri;A. Meluzzi;
2019
Abstract
The tissue injury at the early stages of the heat stress response triggers release of inflammatory and oxidative agents from intestinal content into the milieu of the body. Intestinal homeostasis (i.e., eubiosis) improves the barrier function and mitigates the gut-derived influx of endotoxins. In this study we have analyzed the mitigating role of embryonic stimulation of the gut homeostasis in chickens on immune and oxidative responses to heat. The animal trial was conducted on broiler chickens. The treatment included a single in ovo injection of the galactooligosaccharides (GOS) prebiotic into the air cell of the egg on day 12 of incubation. Control eggs were in ovo injected with the same volume of sterile physiological saline. After hatching, birds were raised in group pens (6 pens/group, 25 birds/pen). Short-term, mild heat stress was induced on day 32 post-hatching by increase in the ambient temperature above the thermal comfort (30 °C for 8.5 h). The spleen was harvested from randomly selected individuals. The relative gene expression study was conducted with RT-qPCR. The two gene panels were analyzed: (1) immune response genes (IL-1β IL-2, IL-4, IL-6, IL-12p40 and IL-17) and (2) stress response genes (HSP25, HSP70, HSP90, BAG3, CAT and SOD). Data were evaluated by the analysis of variance in a 2 × 2 factorial design that included in ovo treatment and ambient temperature as factors. We have found that the immune-related and stress-related gene expression signatures were triggered in animals subjected to heat but with unbalanced intestinal flora (i.e., dysbiotic, without in ovo stimulation with GOS). These animals had increased expression of the genes involved in the immune responses (IL-4 and IL17) and stress responses (HSP25, HSP70, HSP90, CAT and SOD) to short-term heat stress that indicated presence of inflammatory and oxidative mediators (P < 0.05). The individuals that were in ovo stimulated with GOS did not mount the anti-inflammatory or antioxidative responses. Heat shock proteins (HSP25 and HSP70) were increased in both groups challenged with heat, which indicated their role in adaptation to heat.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
