Background: Klebsiella pneumoniae causes severe infections in children, elderly people with poor immunity or in surgical patients, and is associated with an increase in multidrug-resistant bacteria, so the study of K. pneumoniae is more important and needs are increasing. Furthermore, since the infectious agent of K. pneumoniae has not been clearly elucidated, attention has been paid to Outer protein A (OmpA) found in the outer membrane of K. pneumoniae as an infectious agent. OmpA in other Gram-negative bacteria has an evolutionary retention capacity and shows structure and homology in 18 gram-negative intestinal bacteria and intestinal bacteria. OmpA also acts as a surface antigen for the host in Escherichia coli and Yersinia pestis and binds to host cells or to factor H such as immunomodulators, contributing to bacterial toxicity by various mechanisms. Therefore, we perfomed to identify OmpA as an infectious factor in K. pneumoniae. Methods: We performed cell viability analysis, oxidative stress analysis, cell cycle analysis, enzyme-linked immunosorbent assay (ELISA), and Western blotting. Results: The viability of HEp-2 cells was not significantly different with time but the viability of cells decreased by 30% when the concentration of KpOmpA was increased from 10 μg/mL to 60 μg/mL. The production of ROS increased 4 times when the concentration was increased from 10 μg/mL to 60 μg/mL. There was a difference in the cell cycle arrest of HEp-2 cells according to the time and concentration of KpOmpA. When the concentration was increased from 10 ㎍/mL to 60 ㎍/mL at 36 hours, the G2/M phase increased from 21.9% to 51%, confirming the induction of cell cycle arrest at the G2 / M phase via CyclinB1 / cdc2. Inflammatory cytokines of HEp-2 cells increased 1.2 times in IL-6 and mes in IL-8 at KpOmpA 10 μg/mL in 36 hours. Conclusion: These results indicate that KpOmpA affects the host cell and produces ROS, which decreases cell viability and cell cycle arrest in G2 / M phase. It also induces inflammation, a cytokine that acts as an inflammatory reaction.