On the occasion of the World Autism Awareness Day, that will be celebrated on the 2nd of April, WAidid suggests the article 'Multiple inflammasome complexes are activated in autistic spectrum disorders', published on 'Brain, Behavior, and Immunity' (available online from 12 March 2016).

SUMMARY:
Autistic spectrum disorders (ASD) is described in DSM 5 as a neurodevelopmental disorder characterized by persistent deficits in social communication and social interaction across multiple contexts, and restricted, repetitive patterns of behavior, interests, or activities (DSM 5). ASD is associated with psychiatric and non-psychiatric comorbidities that include immune alterations, such as an increased production of proinflammatory cytokines by peripheral blood immune cells and mucosal lymphocytes from the ileal lymphoid tissue. Inflammation was recently shown to be modulated by the activity of the inflammasomes: intracellular multimeric protein complexes whose aggregation leads to the generation of proinflammatory cytokines. The activity of the inflammasomes, the concentration of the inflammasomes-derived proinflammatory cytokines interleukin (IL)-1b and IL-18, and serum parameters of GI damage were analyzed in 25 ASD children, 23 healthy siblings (HS) and 30 unrelated age-matched healthy controls (HC). Results show that the inflammasome system is activated in ASD. Migration of immune cells carrying active inflammasomes and/or of the proinflammatory cytokines produced as a consequence of such activation across the brain blood barrier would likely be an important factor in ASD-associated neuroinflammation. Recent data indicate that this process results in microglial activation, loss of synaptic connections and neuronal cell death: histological findings that are described in autism. If this is the case, therapeutic approaches aiming at reducing inflammasome activity might results in a clinical benefit in ASD. These results show that the inflammasomes are activated in ASD and shed light on the molecular mechanisms responsible for ASD-associated neuroinflammation. The observation that GI alterations could be present as well in ASD offers a possible link between such alterations and neuroinflammation. Therapeutic strategies targeting inflammasome activation could be useful in AS

AUTHOR: Marina Saresella, Federica Piancone, Ivana Marventano, Martina Zoppis, Ambra Hernis, Michela Zanette, Daria Trabattoni, Matteo Chiappedi, Alessandro Ghezzo, Maria Paola Canevini, Francesca la Rosa, Susanna Esposito, Mario Clerici

To read the article online, click here.