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Title:   Author  item
                                            Carroll, Jeffery

                                                         - *Jeff Carroll*
  Submitted to: Journal of Animal Science
                                    Publication Type: Review Article
                                    Publication Acceptance Date: 8/17/2007
                                    Publication  Date: 8/20/2007
                                    Citation: Carroll, J.A. 2007. Bi-directional communication: Growth and immunity in domestic livestock. Journal of Animal Science. 2007-0480v1. doi:10.2527.Interpretive Summary: The existence of communication pathways among various hormonal products of the endocrine system and the immune system has been documented in a variety of species for more than four decades. As early as 1965, investigators revealed a connection between endocrine hormones and the functionality of the immune system. In the 1970’s, researchers were already exploring the mechanistic pathways by which protein hormones could modulate immunity, and had specifically linked growth hormone to cellular immunity, immunological memory, and activation of lymphocytes. This review highlights the established relationships that have been reported between the immune system, primarily the acute phase immune response, and the somatotropic axis in sheep, cattle, and pigs. Hormonal regulation of the immune system and the relationship between immunity and productivity in avian species has been exceptionally well covered by others and therefore are not covered in the present review. Information provided in this review will be of particular interest to researchers seeking to explain the associations between the growth axis and immune system in domestic livestock.
                                Technical Abstract: Evidence continues to mount supporting the existence of bi-directional communication pathways between the animal’s growth axis and immune system. For more than three decades, researchers have sought, and identified, linkages between the somatotrophic axis and health in domestic livestock. Early investigations were particularly interested in the various effects of exogenous growth hormone (GH) on both in vitro and in vivo aspects of immunity in domestic livestock. During an immunological insult, an uncoupling of the GH/insulin-like growth factor I (IGF-I) axis occurs resulting in elevated concentrations of GH in the presence of low circulating concentrations of IGF-I. Typically, sick animals experience a period of anorexia, thus requiring nutrient repartitioning and nutrient sparing to liberate nutrients for the production of proteins such as the pro-inflammatory cytokines and acute phase proteins that are critical for re-establishing homeostasis. While the energy liberating effects of GH are well recognized, the significance of elevated GH during times of sickness-induced anorexia may be more profound due to its stimulatory actions on immune cells. In addition to GH, IGF-I and its associated binding proteins (IGFBP) have also generated significant interest with regard to their interactions with various pro-inflammatory cytokines and the overall effect on muscle growth and repair. For example, recent studies have demonstrated that the pro-inflammatory cytokines interleukin 1-beta (IL-1 beta) and IL-6 can impair IGF-I stimulated muscle growth, and may alter IGFBP profiles thereby indirectly altering the bioactivity of IGF-I (Broussard et al., 2004). In contrast to the catabolic actions of IL-1 beta and IL-6 on muscle tissue, IL-15, a cytokine produced in various tissues including placenta, skeletal muscle, kidney, lung, heart, and macrophages, has been reported to act in an additive fashion with IGF-I on muscle fiber growth (Quinn et al., 1995). Further elucidation of the cross-communication that takes place among the endocrine, neuroendocrine, immune, and nutritional processes within the body will undoubtedly continue to be unveiled as researchers pursue the complexities associated with the regulation of the immune system.


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