ATF3 regulates LPS-induced airway CXCL1 production. (A) WT (white bars) and ATF3^−/− (black bars) mice were challenged i.t. with 10 ng LPS and lavaged 4 hours later. Following lavage, the left upper lung lobes were removed for mRNA quantification by qRT-PCR for (left) Cxcl1 or (right) Cxcl2. Representative of a single experiment, N = 3 to 5 mice/group. (B) The −3-kb region of the Cxcl1 promoter was analyzed using online TESS software to identify the putative ATF3 binding sequence GCA CGT CA (pink box), as well as known NF-κB binding sites (green boxes). (C) WT (white bars) and ATF3^−/− (black bars) mice were challenged i.t. with increasing doses of LPS. After 2 hours, lungs were lavaged, and cell-free supernatants were analyzed by ELISA for (left) CXCL1 or (right) CXCL2. Representative of 3 experiments, N = 2 to 9 mice/group. (D) WT (dotted lines) and ATF3^−/− (solid lines) mice challenged i.t. with 10 ng LPS were lavaged at the indicated times to evaluate (left) CXCL1 or (right) CXCL2 production by ELISA. Representative of 7 experiments; N = 3 to 7 mice/group. Statistics are unpaired 2-tailed Student t test compared with WT control. Data are mean ± standard error of the mean (SEM). *P < .05, **P < .01.