Attenuated ACE2 activity in response to bacterial infection leads to decreased inactivation and increased bioavailability of DABK, resulting in the release of pro-inflammatory mediators such as C-X-C motif chemokine 5 (CXCL5), macrophage inflammatory protein-2 (MIP2), C-X-C motif chemokine 1 (KC), and tumor necrosis factor (TNF)-α from airway epithelia, and increased neutrophil infiltration [27]. The gene discussed is CXCL5; the disease is bacterial infectious disease.