Background: Pulmonary vascular endothelial activation, inflammation, and stress oxidative have been implicated in adverse clinical outcomes of community-acquired pneumonia (CAP). Chronic lung problems such as asthma may affect the consequences of pneumonia.The present study aimed to assess the effects of asthma on the oxidative stress, inflammation, and endothelial dysfunction biomarkers in children pneumonia. Methods: This cross-sectional study was performed at Amir Kabir Hospital affiliated to Arak University of Medical Sciences, Arak, Iran. Participants were 25 children with severe CAP and asthma (group I), 25 children with severe CAP (group II), and 25 healthy children (group III) with 2 to 6 years of age. Fasting blood samples were taken to the assay of serum malondialdehyde (MDA), total antioxidant capacity (TAC), tumor necrosis factor-alpha (TNF-α), soluble vascular cell adhesion molecule-1 (sVCAM-1), and Plasminogen activator inhibitor-1 (PAI-1). Results: We observed a significant reduction in TAC in groups I and II compared with group III. This reduction was significantly higher in group I than in group II. Also, we observed a significant increase in MDA and TNF-α in groups I and II compared with group III. The increase in MDA was significantly higher in group I than in group II. VCAM-1 and PAI-1 as endothelial dysfunction biomarkers increased significantly in group I compared with groups II and III. Also, VCAM-1 and PAI-1 increased significantly in group II compared with groups III. Conclusions: Asthma can exacerbate the consequences of pneumonia in children by increasing oxidative stress, inflammation, and endothelial dysfunction.