Eje Inflamación Sistémica-Neuroinflamación y Desregulación Sensorial en el Trastorno del Espectro Autista: Revisión Sistemática de los Mecanismos Fisiopatológicos

Background: Autism spectrum disorder (ASD) is frequently associated with sensory processing abnormalities and severe sensory crises. Chronic low-grade systemic inflammation and neuroinflammation have recently emerged as key pathophysiological mechanisms underlying these manifestations. Objective: To systematically analyze the scientific evidence on the systemic inflammation–neuroinflammation axis and its relationship with sensory dysregulation and sensory crises in ASD. Methods: A systematic review was conducted according to PRISMA 2020 guidelines using PubMed, Scopus and ScienceDirect databases, including studies published between 2008 and 2024. Meta-analyses, clinical studies, neuropathological investigations, neuroimaging studies and animal models addressing inflammation, neuroinflammation and sensory processing in ASD were included. Results: Meta-analyses consistently demonstrate small-to-moderate but persistent elevations of pro-inflammatory cytokines (IL-6, IL-1β, TNF-α, IFN-γ, IL-8, MCP-1), along with a relative reduction of anti-inflammatory mediators such as IL-10 and IL-1Ra. Functional disruption of the blood–brain barrier, microglial pro-inflammatory activation, reactive astrogliosis and excitatory–inhibitory imbalance are documented. These alterations are associated with central sensory network dysfunction and peripheral sensory receptor sensitization, constituting the neurobiological substrate of sensory crises. Conclusions: Chronic systemic inflammation and low-grade neuroinflammation play a central role in the pathophysiology of sensory dysregulation and sensory crises in ASD. These findings support a paradigm shift toward precision medicine models based on neuroimmune profiling and integrative therapeutic strategies.