Osteoimmunology: A Link between Gastrointestinal Diseases and Skeletal Health in Chickens

Abstract

Bone serves as a multifunctional organ in avian species, giving structural integrity to the body, aiding locomotion and flight, regulating mineral homeostasis, and supplementing calcium for eggshell formation. Furthermore, immune cells originate and reside in the bone marrow, sharing a milieu with bone cells, indicating a potential interaction in functions. In avian species, the prevalence of gastrointestinal diseases can alter the growth and the immune response, which costs a great fortune to the poultry industry. Previous studies have shown that coccidiosis and necrotic enteritis can dramatically reduce bone quality as well. However, possible mechanisms on how bone quality is influenced by these disease conditions have not yet been completely understood, other than the reduced feed intake. On the other hand, several mediators of the immune response, such as chemokines and cytokines, play a vital role in the differentiation and activation of osteoclasts responsible for bone resorption and osteoblasts for bone formation. In the case of Eimeria spp./Clostridium perfringens coinfection, these mediators are upregulated. One possible mechanism for accelerated bone loss after gastrointestinal illnesses might be immune-mediated osteoclastogenesis via cytokines-RANKL-mediated pathways. This review article thus focuses on osteoimmunological pathways and the interaction between host immune responses and bone biology in gastrointestinal diseases like coccidiosis and necrotic enteritis affecting skeletal health.

Keywords: coccidiosis; necrotic enteritis; osteoimmunology; skeletal health.

Figure 1

The mechanism of mesenchymal and hematopoietic cell differentiation into osteoblast and osteoclast, along with the bone remodeling process. RANKL: Receptor activator of nuclear factor κB ligand, RANK: Receptor activator of nuclear factor κB, OPG: Osteoprotegerin, MCSF: Macrophage colony-stimulating factor, CFMS: Colony stimulating factor receptor, H⁺: Hydrogen ion, Cl⁻: chloride ion.

Figure 2

Schematic representation of the interaction between immune responses and bone biology following gastrointestinal disorder (coccidiosis and necrotic enteritis) in chickens. IL-1β: Interleukin 1 β, IL-6: Interleukin 6, IL-12: Interleukin 12, Th1: T helper cells 1 (Cell-mediated immunity), Th2: T helper cells 2 (Humoral immunity), Treg: Regulatory T cells, Th17: T helper cells 17, IFN-γ: Interferon γ, IL-2: Interleukin 2, TNF-α: Tumor necrosis factor α, IL-3: Interleukin 3; IL-4: Interleukin 4, IL-9: Interleukin 9, IL-10: Interleukin 10; IL-13: Interleukin 13; IL-17: Interleukin 17, RANKL: Receptor activator of nuclear factor κB ligand, RANK: Receptor activator of nuclear factor κB, OPG: Osteoprotegerin, MCSF: Macrophage colony-stimulating factor, CFMS: Colony stimulating factor receptor, H⁺: Hydrogen ion, Cl⁻: chloride ion.