Role of macrophage inflammatory protein-1 alpha in wheezy infants

ABSTRACT

To identify the role of macrophage inflammatory protein-1alpha [MIP-lalpha], a member of CC-chemokine subfamily, in the pathogenesis of bronchial hyper-reactivity, peri-bronchial cell infiltration and airway obstruction in bronchial asthma and acute viral bronchiolitis and to correlate its level with the severity of the disease process. 15 asthmatic children and 15 children with acute viral bronchiolitis compared to 15 normal children with matched age and sex. Measurement of plasma MIP-lalpha level by ELISA and Quantitative estimation of total serum IgE by I MX Microparticle Enzyme Immunoassay. The mean plasma MIP-l alpha was significantly higher in asthmatic and acute bronchiolitis cases [93.4 +/- 46.3 pg/mL and 80.7 +/- 34.49 pg/mL, respectively] than in the controls [15.71 +/- 3.3 pg/mL], p value < 0.01. Mean while, MIP-lalpha level showed significant elevation with advanced severity of asthma where it was 64.0 +/- 20.07 pg/mL, 90.86 +/- 30.35 pg/mL and 157.33 +/- 54.55 pg/mL in the intermittent, mild persistent and moderate persistent subgroups. In addition, when the sample member was classified according to the seventy of the attack, MIP-la level was significantly higher in the severe attack [132.7 +/- 48.5 4 pg/mL] than in moderate [72.14 +/- 18.55 pg/mL] and mild attacks [50.0 +/- 4.24 pg/mL], p value < 0.01.In cases of acute bronchiolitis, the mean plasma MIP-lalpha showed positive correlation with the grade of respiratory distress where it was 49.0 +/- 5.70 pg/mL, 83.67 +/- 4.80 pg/mL and 116.0 +/- 46.01 pg/mL in mild, moderate and severe cases, respectively, p value < 0.01. Mean plasma IgE level in asthmatics [195.24 +/- 191.53 IU/mL] was also significantly elevated compared to the controls [12.20 +/- 10.56 IU/mL]. Within the asthmatic group, the mean plasma IgE level correlates positively with the degree of severity of the asthmatic attack. Plasma MIP-lalpha participates in creation of bronchial hyper-reactivity, airway inflammation and obstruction in wheezy infants during asthmatic and acute bronchiolitis attacks. Inhibition of such chemokine effects might be beneficial for designing new therapeutic strategies directed at immunomodulation of bronchial asthma and respiratory syncytial viral bronchiolitis