Infection, immunity and the neuroendocrine response

Abstract

The Central Nervous (CNS) and Immune Systems (IS) are the two major adaptive systems which respond rapidly to numerous challenges that are able to compromise health. The defensive response strictly linking innate to acquired immunity, works continuously to limit pathogen invasion and damage. The efficiency of the innate response is crucial for survival and for an optimum priming of acquired immunity. During infection, the immune response is modulated by an integrated neuro-immune network which potentiates innate immunity, controls potential harmful effects and also addresses metabolic and nutritional modifications supporting immune function. In the last decade much knowledge has been gained on the molecular signals that orchestrate this integrated adaptive response, with focus on the systemic mediators which have a crucial role in driving and controlling an efficient protective response. These mediators are also able to signal alterations and control pathway dysfunctions which may be involved in the persistence and/or overexpression of inflammation that may lead to tissue damage and to a negative metabolic impact, causing retarded growth. This review aims to describe some important signalling pathways which drive bidirectional communication between the Immune and Nervous Systems during infection. Particular emphasis is placed on pro-inflammatory cytokines, immunomodulator hormones such as Glucocorticoids (GCs), Growth hormone (GH), Insulin-like Growth Factor-1 (IGF-1), and Leptin, as well as nutritional factors such as Zinc (Zn). Finally, the review includes up-to-date information on this neuroimmune cross-talk in domestic animals. Data in domestic animal species are still limited, but there are several exciting areas of research, like the potential interaction pathways between mediators (i.e. cytokine-HPA regulation, IL-6-GCS-Zn, cytokines-GH/IGF-1, IL-6-GH-Leptin and thymus activity) that are or could be promising topics of future research in veterinary medicine.

Effects of dietary nucleotide supplementation on growth performance and hormonal and immune responses of piglets

“…In this study, an overall positive correlation was found between cortisol and GH but not between GH and IGF-1 plasma levels; the mean GH plasma level was lower in T1 at day 35. These observations furtherly sustain an uncoupling between the plasmatic levels of GH and IGF-1 and that the level of plasmatic GH could be mainly involved to counteract the levels of cortisol and their negative effect on metabolism and on immune efficiency in weaned piglets (Borghetti et al, 2006a(Borghetti et al, , 2006b(Borghetti et al, and 2009. In this view, the different trend in mean cortisol and GH plasma levels between groups could testify a reduction of the negative effect of stress on growth in T1.…”

Profile of toll-like receptor mRNA expression in the choroid plexus in adult ewes

“…The cellular basis of these barriers is located within the endothelial cells of the microvessels of the brain and the epithelial cells of the CP and arachnoid barrier cells (Skipor and Thiery, 2008). Some ligands of TLRs, such as LPS and poly I:C (TLR3 ligand), do not pass brain barriers; therefore, the localisation of TLRs in structures where these barriers are localised plays a key role in transferring signals from TLRs to the brain (Singh and Jiang, 2004;Borghetti et al, 2009). used in situ hybridisation techniques to provide evidence that the mRNA for TLR4 is present in the circumventricular organs, CP and leptomeninges.…”

Clinical, haematological, cytokine and acute phase protein changes during experimental Babesia gibsoni infection of beagle puppies

“…However, these increases were delayed by more than two weeks following infection and did not develop until after a peripheral parasitaemia was detected. Cytokines are fundamentally involved in the pathophysiology of the systemic inflammatory response to infection (Borghetti et al, 2009;Lewis et al, 2012). The interval between experimental B. gibsoni infection and the cytokine alterations detected in this study indicates that the systemic inflammatory response induced by experimental B. gibsoni infection, like the acute phase response, may be delayed by more than two weeks following infection.…”

“…Cytokines play a critical role in the initiation and M A N U S C R I P T A C C E P T E D ACCEPTED MANUSCRIPT 5 development of systemic inflammation and are responsible for mediating and regulating all aspects of the immune response to infection (Borghetti et al, 2009;Lewis et al, 2012).…”

“…However, while important for host defence, excessive production and release of these immunoregulatory mediators can prove deleterious to the host, initiating widespread tissue injury and organ damage (Borghetti et al, 2009;Lewis et al, 2012). Longitudinal kinetic profiling of a broad range of cytokine alterations that occur during an infection can be useful to expand our understanding of the immunopathogenesis of infectious diseases and hostadaptive humoral and cell-mediated immune responses to infection, as well as potentially allowing the identification of future diagnostic markers and therapeutic interventions.…”