Further studies in a mouse model of OVA-AAI, accompanied by infection with Chlamydia muridarum or Haemofilus influenza, demonstrated an increased expression of NLRP3 in airway epithelial and infiltrating immune cells, as well as enhanced IL-1β and caspase-1 mRNA levels in the lungs of infected mice [184]. The gene discussed is IL1B; the disease is infection.