Abstract
Simple SummaryGalactooligosaccharides (GOS) delivered in ovo stimulate development of indigenous microflora in the chicken embryo. Such stimulation may create a eubiotic environment in the guts which positively influences intestinal function and health. This study aimed to evaluate the impact of GOS delivered in ovo on the modulation of the transcriptomic responses in the intestinal tissues of broiler chickens challenged (or not challenged) with heat in the last growing phase. GOS stimulated several groups of genes in jejunum and in cecum independently of the heat stress provision. A general favourable effect of GOS was recognized due to the enrichment of energetic metabolism-related gene sets, mainly in jejunum. The enrichment of lipid metabolism-related gene sets in the GOS group might have contributed to gut function and barrier maintenance, which might also be linked to a reduced immune system activation, mainly at cecum level. The heat stress impaired gut functions in terms of energy and immunity, in agreement with previous studies. Under heat stress condition, the in ovo injection of GOS did not provide additional benefits to the intestinal transcriptomic response.This study investigated the effects of a galactooligosaccharide (GOS) prebiotic in ovo injected on intestinal transcriptome and plasma immune parameters of broiler chickens kept under thermoneutral (TN) or heat stress (HS) conditions. Fertilized Ross 308 eggs were injected in ovo with 0.2 mL physiological saline without (control, CON) or with 3.5 mg of GOS (GOS). Three-hundred male chicks/injection treatment (25 birds/pen) were kept in TN or HS (30 °C) conditions during the last growing phase, in a 2 × 2 factorial design. At slaughter, from 20 birds/injection group (half from TN and half from HS), jejunum and cecum were collected for transcriptome analysis, and plasma was collected. No differences in plasma parameters (IgA and IgG, serum amyloid) and no interaction between injection treatment and environment condition were found. GOS-enriched gene sets related to energetic metabolism in jejunum, and to lipid metabolism in cecum, were involved in gut barrier maintenance. A homogeneous reaction to heat stress was determined along the gut, which showed downregulation of the genes related to energy and immunity, irrespective of in ovo treatment. GOS efficacy in counteracting heat stress was scarce after ten days of environmental treatment, but the in ovo supplementation modulates group of genes in jejunum and cecum of broiler chickens.
Highlights
Genetic selection for fast-growing and heavy hybrid broilers has halved the duration of rearing [1,2].At the same time, an increasing incidence of stress-induced myopathies and environmental stress susceptibility have been observed [1,3]
Results from plasma Immunoglobulin A (IgA), Immunoglobulin G (IgG) and serum amyloid A (SAA) were analyzed by two-way ANOVA with R software (Stats Package) considering environmental condition (TN or heat stress (HS)) and in ovo injection (CON or GOS) as factors and considering differences statistically significant at p ≤ 0.05
Other gene sets related to metabolic processes were found enriched in GOS, in jejunum
Summary
An increasing incidence of stress-induced myopathies and environmental stress susceptibility have been observed [1,3]. Fast-growing broilers are highly susceptible to heat stress due to the low thermoregulatory capacity, compared to unimproved fowls [5]. The low heat loss capacity, which is partially influenced by the body size, results in thermoregulatory effort with respiratory breathlessness that requires a high metabolic cost, which in turn increases heat production [6]. Besides the impact on meat quality, heat stress strongly affects animal health by inducing oxidative damage to lipid, protein and DNA, leading to endocrine disorders and negative consequences on immune response and increasing inflammatory cytokines and intestinal dysfunction [7,8]. Commensal gut bacteria protect the host from pathogens by stimulating immune responses, competing for epithelial binding sites and producing bacteriocins
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