Sudden infant death syndrome: Postulated role of impaired vasoactive neuropeptide-related inflammatory modulation

Abstract

Sudden infant death syndrome (SIDS) has been extensively investigated in the context of infection as a contributing factor in the death of otherwise apparently healthy infants. A number of infectious agents have been implicated suggesting the causal pathomechanism is related to infection, but not necessarily solely attributable to any one type of infection. An alternative provocative hypothesis is that of post-infection autoimmunity affecting critical novel neurotransmitters of the vasoactive neuropeptide family. Their role in respiratory and cardiac functioning together with novel hypotheses postulating their autoimmune compromise may suggest a role in SIDS etiology following infection. Animal models demonstrate their vital role in neonatal survival and the neuronal control of breathing. Autoimmune compromise of vasoactive neuropeptide receptors through molecular mimicry following infection or idiopathic autoimmunity is postulated as a cause of SIDS.