Abstract
Salmonella challenge leads to systemic responses that induce the hypozincaemia in mice, which is considered a vital strategy against Salmonella invasion. However, it is not yet known if this phenomenon occurs in broilers. To investigate the change in zinc homeostasis of broilers against Salmonella challenge, 1-day-old male broilers were fed with the basal diet for 7 days. Afterwards, broilers were orally inoculated with either 0 or 0.5 × 108 CFU Salmonella Typhimurium (ST). The serum and selected tissues of Salmonella-challenged and non-challenged broilers were collected at 1, 3 and 7 days post-challenge for zinc homeostasis analysis. Our results showed that Salmonella challenge results in hypozincaemia (serum zinc decrease and liver zinc increase) via modulating the systemic zinc homeostasis of broilers. A profound, zinc transporter–mediated zinc absorption and redistribution affecting zinc homeostasis provided a mechanistic explanation for this phenomenon. In addition, we found that the zinc importers Zip5, Zip10, Zip11, Zip12, Zip13 and Zip14 were mainly downregulated in Salmonella-challenged broilers to reduce zinc absorption in the duodenum, while the Zip14 mRNA expression was upregulated to redistribute zinc into the liver. Collectively, these findings reveal that broilers counteract Salmonella infection via modulating their systemic zinc homeostasis.
Highlights
Food-borne Salmonella remains a major public health concern worldwide, being responsible for hundreds of millions of cases of human gastroenteritis [1,2,3]
Our results showed that there was no significant difference in the average body weight between the control and Salmonella-challenged broilers (Fig. 1a), with only a slight tendency towards a decreased body weight of broilers at 14 days (P = 0.0953)
Salmonella challenge resulted in a serum zinc decrease at 3 days post-challenge (Fig. 2a) and a liver zinc content increase, zinc was redistributed into the liver at 1 day post-challenge (Fig. 2b)
Summary
Food-borne Salmonella remains a major public health concern worldwide, being responsible for hundreds of millions of cases of human gastroenteritis [1,2,3]. Hypozincaemia has been observed after acute administration of numerous pathogens and agents, such as Mycobacterium tuberculosis, IL-6 and LPS [16,17,18]. This process is accompanied by a decrease in the serum zinc concentration and an increase in the zinc content in the liver due to the altered activity of zinc transporters, especially upregulation of Zip gene expression [16]. A similar phenotype was observed in broilers under Escherichia coli or LPS stimulation [21] In this context, broilers could use hypozincaemia as a useful defence strategy against pathogen infection. This has not yet been studied in broilers under Salmonella infection, and the roles and mechanisms of hypozincaemia in broilers are largely unknown
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