Location: Livestock Behavior ResearchTitle: Effect of threonine on secretory immune system using a chicken intestinal ex vivo model with lipopolysaccharide challenge Author
|Zhang, Q - Purdue University|
|Chen, X - Purdue University|
|Ajuwon, K - Purdue University|
|Applegate, T - Purdue University|
Submitted to: Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/23/2017
Publication Date: 4/18/2017
Citation: Zhang, Q., Chen, X., Eicher, S.D., Ajuwon, K.M., Applegate, T.J. 2017. Effect of threonine on secretory immune system using a chicken intestinal ex vivo model with lipopolysaccharide challenge. Poultry Science. 0:1-9. doi: 10.3382/ps/pex111.
Interpretive Summary: Gut inflammation is a problem in agriculture species and humans. The amino acid Threonin (Thr) is an important immunological and mucus component during inflammation caused by gram negative bacteria (such as E. coli or Salmonella). Thus those elements are important as the first line of defense against disease in the intestines. We used an ex vivo model using chicken intestines to determine the role of reduced Thr in the inflammatory processes. In vivo Thr deficiency impaired inflammatory and secretory immune responses. Molecular signaling investigations showed that 2 common molecular signals, nuclear factor-kB (NF-kB) and extracellular-regulated protein kinase (ERK), were required for the molecular processes. This work demonstrated the need to keep adequate Thr to maintain gut health and immune responses.
Technical Abstract: Secretory IgA (sIgA) and its transcytosis receptor, polymeric immunoglobulin receptor (pIgR), along with mucus, form the first lines of intestinal defense. Threonine (Thr) is a major constituent component of intestinal mucins and IgA, which are highly secreted under lipopolysaccharide (LPS) induced inflammation. Therefore, the effect of Thr on secretory immune system was determined in an ex vivo chicken ileal explant model. The results showed that 2 h of Thr deprivation from culture medium induced a compensatory increase (P = 0.05) of interleukin-8 (IL-8), MUC2 and IgA mRNA expression in the presence of LPS challenge, suggesting Thr was required for mucin and IgA production under inflammation. However, explants from birds fed Thr deficient diets showed higher IL-8 mRNA expression (P = 0.05) and no change of mRNA expression of MUC2, IgA and pIgR (P > 0.05) at 2 h of incubation, regardless of LPS challenge. Additionally, explants from birds fed Thr deficient diets had no response to Thr deprivation from culture medium (P > 0.05) at 2 h of incubation. These results indicated in vivo Thr deficiency had impaired inflammatory and secretory immune responses. Furthermore, we examined the contributions of nuclear factor-kB (NF-kB) and extracellular-regulated protein kinase (ERK) to expression of MUC2 and pIgR as well as regulation of IgA transcytosis in chicken ileal explant in the stimulation of LPS. The results showed induction of MUC2 genes required both NF-kB and ERK activation, whereas pIgR expression was regulated by complex mechanisms that involved a direct role for the activation of NF-kB and an indirect role for IgA transcytosis mediated by the ERK activation.