Feed-induced gut inflammation and oxidative stress in chickens; what antibiotic growth promoters actually hide

calendar icon 1 December 2020
clock icon 5 minute read

This kind of intestinal disorders are more prominent in chicks previously naive to inflammation-inducing feed ingredients. Therefore, young chicks react through an inflammation response that may end up being complicated by opportunistic bacterial pathogens present in their immature gut. However, when AGP are added to feed, such feed-induced inflammatory responses are mitigated by the anti-inflammatory effect of AGP.

Anti-inflammatory effect of AGP

In recent years, the antimicrobial effect of AGP has been questioned, since the concentrations they reach in the intestinal lumen are sub-therapeutic and therefore lower than the minimum inhibitory concentrations for pathogens. Furthermore, uninterrupted use of AGP induces antibiotic resistance in pathogens. On the contrary, the anti-inflammatory effect of AGP, as their main mechanism of action, has been gaining relevance. What many antibiotics have indeed in common is that they accumulate in inflammatory cells. Consequently, most accumulated antibiotics can inhibit phagocytic inflammatory cells of the innate immune response in the intestine. The relevant outcome of this accumulation in phagocytic cells is the reduction of the inflammatory response. Therefore, the levels of pro-inflammatory cytokines are lower in AGP-treated animals, which in turn will result in lower catabolic inducement, typical of inflammation (Niewold, 2007). In other words, AGP inhibit inflammatory responses that slow the growth of chickens. Therefore, when there is no AGP in the feed, the feed-induced sterile inflammations reemerge. A good strategy will be trying to minimize the occurrence of such feed-induced inflammations beforehand by reducing the amount of dietary stimuli (e.g. ANF) in the basal diet, instead of mitigating them with AGP once they settle down in the intestine (Figure 2).

In conclusion, feed-induced sterile inflammations and oxidative stress in chickens can come from quite a few ingredients. The resulting inflammation-oxidative stress vicious cycle impairs health and performance. Therefore, we should ensure that our AGP-free feed does not contain ingredients that are likely to stimulate inflammation or, at least, we must reduce the amount of anti-nutritional factors in feed as much as possible. This is particularly important in (pre-) starter feed. The sooner we nip the aforementioned vicious cycle in the bud, the better.

Figure 1. Feed-induced inflammation / oxidative stress vicious circle
Figure 1. Feed-induced inflammation / oxidative stress vicious circle

This kind of intestinal disorders are more prominent in chicks previously naive to inflammation-inducing feed ingredients. Therefore, young chicks react through an inflammation response that may end up being complicated by opportunistic bacterial pathogens present in their immature gut. However, when AGP are added to feed, such feed-induced inflammatory responses are mitigated by the anti-inflammatory effect of AGP.

Anti-inflammatory effect of AGP

In recent years, the antimicrobial effect of AGP has been questioned, since the concentrations they reach in the intestinal lumen are sub-therapeutic and therefore lower than the minimum inhibitory concentrations for pathogens. Furthermore, uninterrupted use of AGP induces antibiotic resistance in pathogens. On the contrary, the anti-inflammatory effect of AGP, as their main mechanism of action, has been gaining relevance. What many antibiotics have indeed in common is that they accumulate in inflammatory cells. Consequently, most accumulated antibiotics can inhibit phagocytic inflammatory cells of the innate immune response in the intestine. The relevant outcome of this accumulation in phagocytic cells is the reduction of the inflammatory response. Therefore, the levels of pro-inflammatory cytokines are lower in AGP-treated animals, which in turn will result in lower catabolic inducement, typical of inflammation (Niewold, 2007). In other words, AGP inhibit inflammatory responses that slow the growth of chickens. Therefore, when there is no AGP in the feed, the feed-induced sterile inflammations reemerge. A good strategy will be trying to minimize the occurrence of such feed-induced inflammations beforehand by reducing the amount of dietary stimuli (e.g. ANF) in the basal diet, instead of mitigating them with AGP once they settle down in the intestine (Figure 2).

In conclusion, feed-induced sterile inflammations and oxidative stress in chickens can come from quite a few ingredients. The resulting inflammation-oxidative stress vicious cycle impairs health and performance. Therefore, we should ensure that our AGP-free feed does not contain ingredients that are likely to stimulate inflammation or, at least, we must reduce the amount of anti-nutritional factors in feed as much as possible. This is particularly important in (pre-) starter feed. The sooner we nip the aforementioned vicious cycle in the bud, the better.

Figure 2. Anti-inflammatory effect of AGP and scenarios without AGP
Figure 2. Anti-inflammatory effect of AGP and scenarios without AGP

A: No AGP in feed and inflammation-inducing dietary stimuli
B: AGP in feed and inflammation-inducing dietary stimuli
C: No AGP in feed and reduction of the inflammation-inducing stimuli

References
References
1. Kogut M.H. et al.
(2018) Inflammatory phenotypes in the intestine of poultry: not all inflammation is created equal.. Poult. Sci. 97:2339–2346
2. Chen F. et al
(2011) Soybean-derived β-conglycinin affects proteome expression in pig intestinal cells in vivo and in vitro.. J. Anim. Sci. 89:743–753
3. De Punder K and L. Pruiboom
(2015) Stress induces endotoxemia and low-grade inflammation by increasing barrier permeability.. Front Immunol. 15 May 15
4. Peng C. et al
(2018) Soybean Glycinin- and β‑Conglycinin-induced intestinal damage in piglets via the p38/JNK/NF-κB signaling pathway.. J. Agric. Food Chem. 66: 9534−9541
5. Mavromichalis, I.
(2019) Major dietary sources of oxidative stress and inflammation.
6. Tian T. et al.
(2017) Pathomechanisms of oxidative stress in inflammatory bowel disease and potential antioxidant therapies.. OxiMed & Cellular Longevity. Volume 2017, Article ID 4535194, 18 pages.
7. Lauridsen C
(2019) From oxidative stress to inflammation: redox balance and immune system.. Poult. Sci. 98: 4240-4246.
8. Ducatelle R et al.
(2018) Biomarkers for monitoring intestinal health in poultry: present status and future perspectives.. Vet Res 49:43
9. Niewold T.A.
(2007) The nonantibiotic anti-inflammatory effect of antimicrobial growth promoters, the real mode of action? A hypothesis.. Poult. Sci. 86: 605-609.

Alfred Blanch

Poultry Category Manager at Hamlet Protein A/S (Horsens, Denmark).

Christine Brøkner

Former Technical Manager at Hamlet Protein
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