Abstract

Our early life nutritional environment can influence several aspects of physiology, including our propensity to become obese. There is now evidence to suggest perinatal diet can also independently influence development of our innate immune system. This review will address three not-necessarily-exclusive mechanisms by which perinatal nutrition can program neuroimmune function long-term: by predisposing the individual to obesity, by altering the gut microbiota, and by inducing epigenetic modifications that alter gene transcription throughout life.

Highlights

  • Infants given Bacteroides fragilis supplements early in life have high salivary secretory immunoglobulin A (IgA) and more basal IFN-γ production. They have reduced expression of the pathogen-associated molecular pattern receptor, toll-like receptor (TLR)4, mRNA and an attenuated pro-inflammatory response to stimulation with lipopolysaccharide (LPS) than those not given the B. fragilis supplements (Gronlund et al, 2000; Sjogren et al, 2009). These findings suggest the possibility that early colonization with B. fragilis can accelerate the maturation of the IgA

  • SUMMARY AND FUTURE PERSPECTIVES Clearly, early life diet is essential for programming many aspects of adult physiology, including immune function and later susceptibility to disease

  • The gut microbiome and changes to the epigenetic profile may be particular mechanisms by which early life diet can alter immune function. In conjunction with these mechanisms, early life diet can predispose a subject to obesity, which has its own consequences for long-term immune function

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Summary

Introduction

This review will address three not-necessarily-exclusive mechanisms by which perinatal nutrition can program neuroimmune function long-term: by predisposing the individual to obesity, by altering the gut microbiota, and by inducing epigenetic modifications that alter gene transcription throughout life. PERINATAL NUTRITION CAN PROGRAM CHANGES IN IMMUNE FUNCTION THAT ARE INDEPENDENT OF ADIPOSITY We can conclude from these studies there is an obvious connection between early life events programming an increased propensity to obesity and obesity itself resulting in a basal proinflammatory profile and susceptibility to infection.

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