# Gut–Brain Inflammation and Disrupted Homeostasis Due to Activation of Mast Cells and Microglia

## TL;DR

The paper explores how gut and brain inflammation caused by mast cells and microglia activation may contribute to Autism Spectrum Disorder, and suggests ways to address these processes.

## Contribution

The paper novelly connects environmental and pathogenic factors to gut-brain inflammation via mast cells and microglia activation in ASD.

## Key findings

- Environmental and pathogenic toxins may disrupt gut and brain barriers through mast cell and microglia activation.
- Chronic gut-brain inflammation could lead to epigenetic effects and increased ASD susceptibility.
- Simple interventions may help address key processes in ASD pathogenesis.

## Abstract

Recent data from the Centers for Disease Control (CDC) indicate that the incidence of Autism Spectrum Disorder (ASD), a neurodevelopmental disorder characterized by deficits in social communication and the presence of restricted interests and repetitive behaviors, has increased to 1 in 31 children. Individuals with ASD have a constellation of neurological, behavioral, sensory, feeding, gastrointestinal, and immunological issues. Even though there is some genetic component to the pathogenesis of ASD, accumulation of environmental and pathogenic toxins could contribute to disruption of the gut–blood-barrier (GBB) and blood–brain barrier (BBB) via activation of mast cells (MCs) and microglia, resulting in a chronic cycle of gut–brain inflammation. Here we discuss how various environmental, pathogenic, and stress factors can disrupt gut–brain homeostasis to create susceptibility and epigenetic effects that contribute to the development of ASD. We also suggest simple ways to address some of the key pathogenetic processes involved in ASD.