Early life stress predisposes to food allergy via modulation of the brain-gut-axis

Abstract

The neural, immune and endocrine pathway communication between the brain and the gut, is referred to as the brain-gut-axis. The brain-gut-axis is a complex reflex network between the central nervous system and the enteric nervous system in the gut, via which the brain can communicate with the gastrointestinal tract. Proper brain-gut-axis functioning is necessary to maintain homeostasis. Early life stress is able to disturb this homeostasis and cause brain-gut-axis dysfunctioning. The early environment in life is extremely important, as both the nervous system and the immune system are still in development. Therefore, exposing the developing nervous and immune systems to stress in early life, can cause long lasting effects which can predispose to disease development. Early life stress is able to affect different aspects of the brain-gut-axis. It leads to changes in different neurotransmitters and neuropeptides (such as serotonin, acetylcholine, CRF and NGF), and causes hyperactivity of the HPA axis with increases in ACTH and corticosterone and a decreased acute stress response. Furthermore, early life stress is able to affect the mucosal immune system in the gut and modulate the epithelial barrier function in different ways. Changes are also found in microbiota composition after early life stress. These changes in the gut microbiota can also lead to changes in the epithelial barrier function. Intestinal barrier dysfunction including altered gut permeability, increases the susceptibility to food allergen sensitization in the gastrointestinal tract, possibly inducing food allergy. In conclusion, early life stress leads to dysfunction of many aspects of the brain-gut-axis. Especially modulation of the gut microbiota and the epithelial barrier permeability, can predispose to the development of food allergy.