Keel Fracture Causes Stress and Inflammatory Responses and Inhibits the Expression of the Orexin System in Laying Hens.

Haidong Wei,Hongwei Xin,Jun Bao,Jianhong Li,Runxiang Zhang,Chun Li,Shuang Li,Xiang Li,Yanju Bi

doi:10.3390/ani9100804

Abstract

Simple SummaryKeel fracture is an important health and welfare problem in laying hens in all production systems. Previous studies have shown that keel fracture can influence hens’ behavior, reduce production performances, and cause pain in laying hens. Additionally, keel fracture also affects their feed intake. However, it is not clear whether the keel fracture induces stress, inflammation, or influences the orexin systems in laying hens. Orexin, also called hypocretin, is associated with the regulation of feed intake, energy homeostasis, and metabolism in poultry animals. Therefore, this study aimed to investigate the effects of keel fracture on stress and inflammatory responses and the activity of the orexin system of laying hens. Our results indicate that keel fracture not only induced stress and inflammatory responses, but inhibited the activity of the orexin system in laying hens. This study provides insights into the adverse effects of keel fracture on laying hens.Keel fracture has negative effects on the health and welfare of laying hens. We investigated effects of keel fracture on stress, inflammation, and the orexin system in laying hens. Ninety 17-week-old Lohmann white laying hens were palpated and euthanatized at 42 weeks old, and marked as normal keel (NK)/fractured keel (FK) from absence/presence of keel fracture. Serum, brain, liver, and abdominal-muscle samples were collected from 10 NK and 10 FK hens to determine the stress and inflammatory responses and the activity of orexin systems by corticosterone content, expression of heat shock proteins (TNF-α 60, 70, 90), and inflammatory factors (tumor necrosis factor (TNF)-α, nuclear factor-kappa Bp65 (NF-κBp65), inducible nitric oxide synthase (iNOS), prostaglandin E synthases (PTGEs), cyclooxygenase-2 (COX-2), interleukin-1β (IL-1β)), orexin (ORX), and orexin-receptor 1/2 (ORXR1/ORXR2). The FK hens had higher serum corticosterone content, Hsps, and inflammatory factor mRNA expression levels than NK hens, although levels of iNOS in the liver and TNF-α in the muscle were similar. Protein levels of Hsp70 and Hsp90 in the brain and liver, iNOS and COX-2 in the liver, NF-κBp65, iNOS, and COX-2 in the brain of FK hens were increased compared with NK hens. Furthermore, FK hens had lower mRNA expression of ORX, ORXR1, and ORXR2 than NK hens. Therefore, keel fracture causes stress and inflammation, and inhibits the expression of the orexin system in laying hens.

Highlights

Keel fracture is an important problem in welfare and health in modern production systems of laying hens
In rat tibia and human femur models, fracture induces pain, stress, and inflammatory responses [10,11]; we do not know whether this response can be seen in laying hens with keel fracture
Studies have reported that acute heat and cold stress upregulate the expression of Hsp60, Hsp70, and Hsp90 [15,16]

Summary

Introduction

Keel fracture is an important problem in welfare and health in modern production systems of laying hens. The inflammatory response induced by fracture occurs mainly in the initial stage of healing, and plays a pivotal role in early repair [17]. Inflammation cytokines, such as tumor necrosis factor-alpha (TNF-α), nuclear factor-kappa B (NF-κB), cyclooxygenase-2 (COX-2), prostaglandin E synthases (PTGEs), and interleukin-1β (IL-1β), are produced at the fracture site. Their players are involved in the regulation of inflammatory response, renewing and differentiation of mesenchymal progenitor cells, as well as in the promotion of fracture healing [18,19,20]. Hsps and inflammatory cytokines play a vital role in the recovery of tissue damage

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