Expression data from uninfected and pneumococcus-infected wt and PGLYPR4-KO primary alveolar epithelial cells

Streptococcus pneumoniae is the most frequent cause of community-acquired pneumonia. Endogenous antimicrobial proteins such as PGLYRP4 might participate to the course of the disease. PGLYRP4 is expressed in different cell types but is downregulated in alveolar epithelial after stimulation with Streptococcus pneumoniae. Interestingly, mice lacking PGLYRP4 displayed an enhanced bacterial clearance in the lungs and less mice develop a bacteremia. This may depend on a higher proinflammatory cytokine response in PGLYRP4KO compared to wt cells, which contribute to the recruitment of more immune cells to the side of infection and an enhanced bacterial clearance by additionally stronger activation of the phagocytes. We implemented microarray analysis of infected primary epithelial cells to identify possible regulated genes by PGLYPR4-deficency, which contribute to the seen phenotype. We isolated primary alveolar epithelial cells from untreated 10-16 week old BALB/c wt and PGLYRP4-deficient mice. We used three mice of each strain and performed three indipendant experiments. The extracted RNA was pooled and analyzed