SUMMARY Although autism spectrum disorder (ASD) is defined by core behavioral impairments, gastrointestinal (GI) symptoms are commonly reported. Subsets of ASD individuals display dysbiosis of the gut microbiota, and some exhibit increased intestinal permeability. Here we demonstrate GI barrier defects and microbiota alterations in a mouse model displaying features of ASD, maternal immune activation (MIA). Oral treatment of MIA offspring with the human commensal Bacteroides fragilis corrects gut permeability, alters microbial composition and ameliorates ASD-related defects in communicative, stereotypic, anxiety-like and sensorimotor behaviors. MIA offspring display an altered serum metabolomic profile, and B. fragilis modulates levels of several metabolites. Treating naïve mice with a metabolite that is increased by MIA and restored by B. fragilis causes behavioral abnormalities, suggesting that gut bacterial effects on the host metabolome impact behavior. Taken together, these findings support a gut-microbiome-brain connection in ASD and identify a potential probiotic therapy for GI and behavioral symptoms of autism.

Background Pediatric patients undergoing cardiopulmonary bypass (CPB) often require blood component transfusions. Pathogen‐reduction (PR) of platelets reduces the risk of microbial contamination; however, its effect on hemostatic efficacy in this population is unclear. This study sought to characterize the hemostatic efficacy of PR platelets in children undergoing CPB. Study Design and Methods We performed a retrospective chart review of patients admitted to a pediatric intensive care unit following CPB surgery from 2015 to 2019. Demographic data, validated scoring of repair complexity, products received, and outcomes were compared. The primary outcome was postoperative chest tube bleeding. Results A total of 140 patients were enrolled. The majority of surgeries (124/140) were Risk Adjustment for Congenital Heart Surgery (RACHS) 1–3 repairs. Seventy‐four percent of patients (104/140) received only standard platelets whereas 26% (36/140) received PR platelets. There were no differences between the groups in the age (p = .90), sex (p = .20) or RACHS score (p = .06). Postoperatively, there was no difference in the median chest tube output for 1 h (p = .27), 2 h (p = .26), 4 h (p = .09), 8 h (p = .16), or for the first 24 h following surgery (p = .23) in patients who received standard versus PR platelets. There was also no difference in receipt of platelets (p = .18), cell saver (p = .79), or cryoprecipitate (p = .28). Conclusion Patients receiving PR platelets did not have more blood loss or require more transfusions than those who received standard platelets. This suggests that PR platelets may provide acceptable hemostasis with the additional benefits of reduced risk of microbial contamination in pediatric patients undergoing CPB.