Location: Food and Feed Safety ResearchTitle: Tissue-, age- and dose-dependent changes in avian ß-defensin and LEAP2 mRNA abundance in the intestines of Salmonella Typhimurium challenged broilers
|GARCIA, JAVIER - Virginia Tech|
|Byrd Ii, James - Allen|
|WONG, ERIC - Virginia Tech|
Submitted to: Animal Biotechnology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/2/2020
Publication Date: N/A
Interpretive Summary: Salmonella is a bacterium commonly found in the gut of chickens. Although Salmonella may cause illness in humans, chickens may not get sick when they have the bacteria. The objective of this study was to evaluate the effects of Salmonella on different peptides that are used in the chicken to fight off the disease caused by Salmonella. On the day the chickens hatched, they were given over a million Salmonella by mouth. Highly specialized tests revealed that there were dose-, type of tissue-, and age- specific changes in the peptides tested. These results demonstrate that Salmonella infection caused an increase in the genetic material of one peptide (Avian beta defensins), but the genetic material decreased at later times. This may be one way that Salmonella avoids the immune system in humans and chickens.
Technical Abstract: Salmonella is a pathogen commonly found in the gastrointestinal tract of poultry. Although Salmonella may cause illness in humans, poultry may show no signs of infection. The objective of this study was to evaluate the effects of Salmonella challenge on the mRNA abundance of host defense peptides (HDP) such as the avian beta defensins (AvBD1, 6, 8, 10, 11, 12, 13) and liver-expressed antimicrobial peptide 2 (LEAP2). On day of hatch, chicks were challenged with one of three levels (10**6, 10**7, 10**8 colony-forming units, cfu) of Salmonella Typhimurium. Quantitative PCR analysis revealed that there were dose-, tissue- and age- specific changes in the abundance of AvBD and LEAP2 mRNA. An initial HDP response was observed only in the 10**8 cfu group with an upregulation of AvBD1, 8, 10, and 12 mRNA on 1-day post infection (dpi). The upregulation of AvBD was transient, since the effect had mostly disappeared by 2 dpi. At 5 and 7 dpi there was an opposite effect with downregulation of AvBD mRNA. At 5 dpi, all seven AvBD mRNA were downregulated in the ileum, while only AvBD1, 6, 10, and 11 mRNA were downregulated in the jejunum and AvBD6, 8, 10, 12, and 13 were downregulated in the cecum. At 7 dpi, there was downregulation of all seven AvBD mRNA in the duodenum and downregulation of some AvBD in the jejunum, ileum, and cecum. LEAP2 was downregulated at all doses of Salmonella in the cecum at 1 dpi and in the ileum at 5 dpi. These results demonstrate that Salmonella infection caused an initial upregulation of AvBD mRNA, but at later times AvBD mRNA was downregulated. This may represent a mechanism that Salmonella uses to evade the immune system.