Perturbation ofcommensal bacteriabyantibioticexposure aggravates ovalbumin (OVA)-induced allergic asthma in pre-weaning mice. However, the influence ofdysbiosisof commensal bacteria on asthma development in post-weaning mice is still limited. Here, we treated 3-week-old post-weaning mice with antibiotics to disrupt commensal bacteria and then established OVA-induced allergic asthma by peritoneal sensitization using OVA/alum andintranasalchallenge with OVA. Contrary to the protective function in pre-weaning mice, commensal bacteria in post-weaning mice aggravated OVA-induced asthma. Commensal bacteria in post-weaning mice promoted OVA-induced allergic asthma through maintenance of NLRP3/IL-1β expression in peritonealmacrophages(pMφ), which promoted recruitment ofinflammatory cells, especially inflammatorymonocytes, into the peritoneal cavity after OVA/alum sensitization. Further study showed that metronidazole- and vancomycin-sensitive bacteria are involved in maintenance of NLRP3/IL-1β signal in pMφ. Our results suggest that certain species of commensal bacteria in post-weaning mice aggravate OVA-induced allergic asthma through NLRP3/IL-1β signal pathway.