In line with these similar defects in bacterial clearance, there was reduced intrapulmonary production of GM-CSF, chemokine (C-X-C motif) ligand 2 (CXCL2), and CXCL1, critical signaling molecules in the innate response to respiratory infection, in antibiotic-treated mice infected with S. pneumoniae (Fig. 1e–g) or K. pneumoniae (Fig. 1h–j). This evidence concerns the gene XCL2 and respiratory tract infectious disorder.