Mucosal airway inflammation is currently considered to be the central element in the pathophysiology of bronchial hyper-responsiveness. However, airway inflammation and bronchial hyper-responsiveness [BHR] do not always correlate. To reevaluate this concept, 20 asthmatic patients and 10 matching control subjects were subjected to pulmonary function tests and blood samples were withdrawn to determine copper, zinc, iron and soluble interleukin-2 receptors [sIL-2R], as markers of inflammation. Although the pulmonary functions of the asthmatic were within normal range, yet they were significantly deviated from their matching control values. Regarding the serum level of sIL-2R, the present results showed a significant elevation of this marker in asthmatic patients when compared to controls. The present data revealed that serum Cu was significantly higher in patients with respect to control subjects. Although serum zinc level was lower in patients than in control subjects, the difference was insignificant. No significant difference in serum Iron level was detected between asthmatic and control groups. No significant correlation was found between bronchial responsiveness, detected by prevocational doses of meth choline [PD_20-FEV1] and any measured marker of inflammation [so IL-2R, Cu, Zn and Fe] and thus, airway inflammation and bronchial hyper-responsiveness do not always correlate. So it can be concluded that airway hyper-responsiveness is not a direct consequence of inflammation and other factors rather than inflammation may contribute to bronchial hyper-responsiveness, as airway remodeling.