Asthma, a prevalent respiratory disorder, is distinguished by airway obstruction and respiratory distress stemming from acute and chronic pulmonary inflammation. In this study, 150 sputum and nasopharyngeal swabs were collected from asthma patients, comprising 87 males and 63 females, specifically to isolate Klebsiella pneumoniae (K. pneumoniae). Additionally, blood samples were obtained from 35 patients at the Allergic Specialized Center, Baghdad, and 25 healthy individuals served as controls. All diagnoses were established by specialist respiratory physicians, and serums were preserved for later serological testing. A sandwich enzyme-linked immunosorbent assay was employed to ascertain the levels of total IgE, IL-4, and IL-22.The pathophysiology of bronchial asthma is intertwined with T-cell activation and fluctuations in cytokine levels. It was hypothesized that serum levels of total Immunoglobulin E (IgE) would be elevated in patients. Indeed, significant differences (p=0.001) were observed between patients' total IgE serum levels (304.33 ± 21.3 IU/mL) and controls (36.54 ± 0.69 IU/mL). Conversely, IL-4 and IL-22 levels in asthma patients (66.77 ± 4.1 pg/mL and 41.83 ± 0.37 pg/mL respectively) differed significantly from healthy controls for IL-4 (22.75 ± 0.68 pg/mL, p<0.01) but not for IL-22 (40.89 ± 1.35 pg/mL). Klebsiella pneumoniae was isolated from 12 sputum and nasopharyngeal swab samples from asthmatic patients. Postincubation, 83.3% of the isolates were found to be biofilm-forming, while 16.7% did not form biofilms. Iron oxide nanoparticles, with an average diameter of 85.9 nm, were utilized to inhibit K. pneumoniae biofilm formation. At a concentration of 5 mg/mL, these nanoparticles exhibited a significant augmentation of about 58% (p≤0.05) in inhibiting biofilm formation. However, at concentrations of 0.5mg/mL and 50 mg/mL, the augmentation was 42.9% (P>0.05) and 37.1% (p>0.05) respectively, which were not statistically significant.This study underscores the potential of iron oxide nanoparticles in impeding biofilm formation by K. pneumoniae and the pivotal role of cytokine levels in the pathophysiology of asthma.