Juxing Chen and Mercedes Vázquez-Añón*
The poultry industry seeks for ways to improve efficiency and cost of production. One way to improve efficiency is to optimize the nutrition and management of the breeder hen to improve reproduction and the performance of the progeny. In the last five years new research has provided evidence on how micro nutrients in the breeder hen diet can improve the immune system of the progeny, providing new opportunities to help the chick develop the immune system, in the face of the antibiotics ban. Zinc and specially in its chelated form fed to breeder hen is effective at improving livability of the young chick, by modulating the cellular and humoral immune response to pathogenic challenges. With recent advances in epigenetics, we better understand the underlying mechanism by which maternal Zn can modulate gene expression of the chicks and improve immune development. Increasing levels of Zn in the diet and in the form of chelates improves storage of Zn in the egg yolk and albumen and more Zn is available for embryo development. In the gut, Zn improves gut barrier function, mucosal and systemic immunity, and reduced gut inflammation of progeny chicks by epigenetic modification of anti-inflammatory proteins, and chelated Zn is more consistent and effective than inorganic Zn. Feeding Zn, especially in the chelated form, to broiler breeders improves livability of the progeny due to a more developed immune system.
Introduction to breeder nutrition
Reviews by Kidd (2003) and Callini & Sirri (2007) summarized the breeder nutrition studies published in the literature. There are two aspects of progeny development that can be improved via maternal nutrition, one is growth performance and carcass yield, and the other one is the health and immunity of the progeny (Callini and Sirri, 2007). Optimizing the levels and type of energy in the breeder diet improved carcass yield of the progeny (Lesson and Summer (2001, and Peebles et al (1999, 2002a)) It has been postulated that hen nutritional programs that increase yolk weight over egg weight provide more energy and protein to the chick posthatch and support faster growth of the offspring, especially in fast growing male broilers. Vitamins and minerals supplementation in breeder hen diets improve livability and immunity of the progeny (Callini and Sigri, 2007). Supplementation of Zn has been shown to improve humoral and cellular immunity and help the progeny response to pathogenic challenges (Kidd 1992 and 1993). Combination of Zn and Mn improved livability of the progeny (Virden et a., 2003).
Epigenetics and Progeny Immunity with Zinc
New advances in epigenetics has helped us better understand the mechanism by which maternal nutrition can impact progeny development. Epigenetics is an important regulatory mechanism of gene expression independently of DNA sequence. There are three types of epigenetic modifications: 1) DNA methylation, which causes DNA-histone compaction and represses gene expression; 2) histone modification in which histone acetylation causes DNA-histone relaxation and activates gene expression and 3) organization of nucleosome along DNA. Recent studies have further our understanding of the mechanism by which maternal nutrition could impact the health of the progeny via epigenetics.
In chickens the adaptive immune system is functionally immature and newly hatched birds are dependent on maternal antibodies transferred through the egg yolk. Zinc has been associated with different aspects of the immune system and maternal Zn could improve the development of the immune system of the off-spring. Li et al., (2015) evaluated the role of maternal zinc on intestinal immunity of the offspring and the underlying epigenetics mechanism in broiler chickens. In this study, broiler breeder hens were fed two levels of two sources of Zn (chelated Zn-MHA and inorganic ZnSO4) for 8 weeks. The progeny chicks from those hens were fed either low (20 ppm) or normal (70 ppm) of inorganic Zn for 6 weeks. Zinc content in the egg yolk and albumen gradually increased with dose and was higher in the yolk than albumen and in the chelated Zn treatments, suggesting further delivery of Zn to the progeny by the chelated Zn. To address gut immune development jejunal secretory IgA (sIgA) and mucin 2 gene expression (MUC2), and serum immunoglobulin Y (IgY) and antibody titers responses against several diseases (New castle and bursal virus) were measured. Compared to Zn deficient or inorganic Zn treatments, Zn-MHA supplementation to breeder hens enhanced mucosal immunity by increasing secretory IgA production in progeny chicks either low or normal Zn diet (Figure 1A); 2) improved gut barrier function by increasing MUC2 gene expression (Figure 1B); 3) enhanced systemic immunity in progeny birds by increasing concentration of IgY in offspring chicks at 1 d of age and antibody titer of NDV and IBDV in offspring chicks at 28 d of age (data not shown). These results suggest that Zn-MHA supplementation in breeder diet is more effective than inorganic Zn at improving gut barrier function, mucosal immunity and systemic immunity of progeny chicks.
Figure 1. Jejunal secretary IgA (sIgA) production and mucosal MUC2 gene expression in offspring chicks at 35 d of age hatched from breeder hens supplemented with 0, 50, 300 ppm CuSO4 or 50, 300 ppm Zn-MHA. Treatments with different letters were significantly different (P < 0.05).
The authors also measured DNA methylation and histone acetylation of A20, an anti-inflammatory protein that negatively regulates nuclear factor κB (NF-κB) signaling pathway, which is one of the major pathways to regulate inflammation that can be induced by external stimuli such as bacteria. Up regulation of A20, down regulates NF-κB pathway, which will reduce inflammation (Figure 2). Chelated Zn supplementation to breeder hens exhibited greater effect than ZnSO4 in 1) reducing gene expression of NF-κB p65 and IL6 (Figure 3 A and B); and 2) increasing A20 gene expression in progeny jejunum (Figure 3C). A20 is a negative regulator of NF-κB pathway, increase of A20 is consistent with reduction of NF-κB p65. These results suggest that Zn-MHA in breeder diets reduced gut inflammation in progeny birds by up-regulation of A20 expression and down regulating NF-κB. These findings were corroborated with DNA methylation and histone acetylation measurements at A20 promoter region. Zn-MHA and ZnSO4 significantly reduced DNA methylation at A20 promoter. Zn-MHA but not ZnSO4 significantly increased histone acetylation at A20 promoter. Because methylation repress gene expression and histone acetylation activate gene expression, reduction of methylation and increase of histone acetylation at A20 promoter region by breeder Zn supplementation will up-regulate A20 gene expression, which is consistent with increase of A20 mRNA levels.
Figure 2. NF-kB signaling pathway in intestinal inflammation
Figure 3.. Zn supplementation in broiler breeder hens and offspring birds increased A20 gene expression and reduced NF-κB and IL6 gene expression in jejunum of offspring birds at 35 d of age. Treatments with different letters were significantly different (P < 0.05).
In summary, Zn supplementation in breeder hens improved gut barrier function, mucosal immunity and systemic immunity and reduced gut inflammation of progeny chicks by epigenetic modification of A20 promoter, and chelated Zn (Zn-MHA) is more consistent and effective than ZnSO4.
References available upon request.