The autism spectrum disorder (ASD) is a group of pathologies characterized by social impairment and restricted and repetitive behaviors. Currently, the etiology of this disorder is not well understood. Our lab has validated a pharmacological model where mice prenatally exposed to Valproic Acid express ASD-related behaviors, along with higher glucose metabolism and increased cFos activity in the Piriform Cortex (PIR). Also, peripheral and brain inflammation have been associated with ASD. In this experiment, we aimed to understand whether an acute inflammatory insult in the PIR may alter the sociability of mice. First, we performed a three-chambered social interaction and novelty test (SI+SN) to assess the basal sociability levels of naive C57BL/6J mice. One week after, through stereotaxic surgery, we administered Lipopolysaccharide (LPS) bilaterally in the PIR, to elicit an acute inflammatory response. Twenty-four hours after surgery, we performed a new SI+SN test. We found that LPS completely abolished both the preference for the social side and for the social novelty. We aim to further characterize the effects of LPS on neuroinflammation, neuronal activity, and integrity of the PIR.