NLRP3 and bacterial infectious disease: In osteomyelitis, increased levels of IL1β expression act cohesively with IL1-α to increase NLRP3 inflammatory vesicles and immune and inflammatory responses through multiple downstream mechanisms.[29] Bacterial infection delays diabetic wound healing and rapidly promotes the expression of the pro-inflammatory gene IL1β in the wound, which tends to be involved in the regulation of IL-6 and TNF-α and the expression of the vascular adhesion molecule ICAM1.[30]