In this article, we aim to illustrate the various possible mechanisms that play a role in the multi-faceted neuroinflammation seen in Autism Spectrum Disorders, which involve the gastrointestinal, immune and nervous systems. As with other environmentally-induced autoimmune disorders, autism is a combination of genetic susceptibility, environmental triggers and barrier dysfunction. The pathogenesis of autism can take many avenues, from gut dysbiosis, to loss of intestinal barrier integrity, to systemic inflammation, to breach of the blood-brain barrier, to neuroinflammation and neuroautoimmunity. The gut-brain axis has been shown to play an important role in the induction of neuroautoimmune disorders.

The connective inter-relation between gut and brain means that dysfunctions or damage to the intestinal barrier or blood-brain barrier can seriously affect one or the other. Environmental triggers actually begin their assault while someone is still in the womb; studies have shown that the efficiency of a person’s immune system or his susceptibility to autoimmune disease can be affected by prenatal conditions, maternal exposures, and continuing exposure throughout a person’s lifetime. Toxic chemicals abound in all aspects of existence, from food to medication to packaging to pollution. Individuals may be immune-reactive to particular chemicals bound to human tissue or food proteins. Infections can affect the immune system and breach the immune barriers.

The triggering factors may also bind to human tissue, including neural tissue, causing tissue reactivity and neuroautoimmunity. By understanding the mechanisms by which these environmental triggers lead to neuroautoimmunity, clinicians may be able to identify the triggers, remove them from a patient’s environment, and devise protocols to repair the barriers and improve the patient’s health.