Location: Livestock Behavior ResearchTitle: Effect of threonine deficiency on intestinal integrity and immune response to coccidiosis in broiler chicks Author
|Zhang, Q - Purdue University|
|Chen, X - Purdue University|
|Ajuwon, K - Purdue University|
|Applegate, T - Purdue University|
Submitted to: British Journal of Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/16/2016
Publication Date: 12/20/2016
Citation: Zhang, Q., Chen, X., Eicher, S.D., Ajuwon, K.M., Applegate, T.J. 2016. Effect of threonine deficiency on intestinal integrity and immune response to coccidiosis in broiler chicks. British Journal of Nutrition. 116:2030-2043. doi:10.1017/S0007114516003238.
Interpretive Summary: Threonine is a nutrient that integrates gut health integrity and the associated immune system. The mucosal layer of the gut is particularly reliant on sufficient threonine. Coccidiosis is a ubiquitous poultry intestinal parasite disease that is difficult to control. Feed withdrawal and threonine deficiency together reduced gain, increased the permeability or leaking of the gut, and reduced a number of immune responses that allow for a robust immune response to the coccidian vaccine challenge. The overall effect was that the threonine deficiency worsened the detrimental effects of the live vaccine challenge on growth performance, increased coccidia egg shedding because of impaired intestinal morphology, reduced barrier function including antibodies in the intestine, and altered immune profiles indicating immune suppression. Therefore, sufficient threonine is critical to support gut health of broiler chicks.
Technical Abstract: For this study, threonine (Thr) deficiency was hypothesized to exacerbate the intestinal damage induced by feed withdrawal and coccidiosis infection because of its high obligatory requirement of the gut. Two dietary Thr treatments (0.49 and 0.90%) were fed to chicks from 1-21 d of age. At 13 d of age, feed was withdrawn for 24 h from half of the birds for each treatment with subsequent gavage of a 25× recommended dose of Coccivac®-B. Thr deficient birds had 38% lower 13-21 d BW gain under combined challenge (Thr × challenge, P = 0.03). At 21 d, the challenged group fed low Thr had higher number of oocysts (+40%, P = 0.03) but lower crypt depth (-31%, P < 0.01), indicating intestinal epithelial proliferation may be a plausible mechanism for oocyst expulsion. Additionally, birds fed low Thr diet had higher gut permeability as measured after 2 h administration of FITC-dextran (3-5 kDa, P < 0.01), which may be attributed to decreased IgA production (P = 0.03) in the ileum. In the cecal tonsils, Thr deficient birds had a limited proliferation of CD3 lymphocyte (49% of Bu-1 lymphocytes) under infection (Thr × challenge, P = 0.09), along with lower CCR9 mRNA primarily expressed on gut homing T cells (P = 0.04). Also, Thr deficiency tended to decrease IFN-' but increased IL-10 mRNA expression induced by coccidiosis (P = 0.09). Overall, Thr deficiency worsened the detrimental effects of coccidiosis on growth performance and oocyst shedding by impairing intestinal morphology, barrier function, lymphocyte profiles and their cytokine expression Therefore, adequate threonine is essential to maintain broiler chick gut health.