EFFECT OF A BRONCHIAL PROVOCATION TEST WITH HOUSE-DUST MITE ON BLOOD EOSINOPHILIA, EOSINOPHIL CATIONIC PROTEIN, SOLUBLE INTERLEUKIN-2 RECEPTOR, AND INTERLEUKIN-6 IN ASTHMATIC-CHILDREN

Eighteen children with perennial asthma and allergy to house-dust mite (HDM) underwent a bronchial challenge with HDM. Before and 24 h after the test, a venous blood sample was taken to determine levels of eosi nophils, eosinophil cationic protein (ECP), soluble interleukin-2 rece ptor (IL-2R), and interleukin-6 (IL-6). A histamine challenge was perf ormed before and 24 h after the HDM challenge. All subjects showed an immediate asthmatic reaction (IAR). A definite late asthmatic reaction (LAR) was observed in 15 children, a probable LAR in two, and no LAR in one. Because of persistent bronchial obstruction (FEV1 < 70 eight c hildren were unable to perform a histamine challenge 24 h after the al lergen challenge. These were the children with the lowest prechallenge provocation dose (PD20) of histamine. In the other 10 children, the m ean PD20 histamine decreased after the HDM challenge (mean PD20 before was 0.56 mg/ml; after challenge it was 0.14 mg/ml; P = 0.007). After the HDM challenge, an increase was detected in the mean values of bloo d eosinophils (mean before was 446/mm3; mean after was 733/mm3; P = 0. 002), ECP (mean before was 26.3 mug/l; mean after was 34.3 mug/l; P < 0.040), and IL-2R (mean before was 116.35 U/ml; mean after was 128.52 U/ml; P < 0.040). On the other hand, IL-6 remained unchanged after the HDM challenge (mean before was 9.47 pg/l; mean after was 9.70 pg/l; P = 0.360). Furthermore, as compared with a group of normal, age-matche d children (n = 18), asthmatic children were found to have higher prec hallenge levels of ECP (mean: 10.3 mug/l compared with 26.3 mug/l) (P < 0.001) and IL-2R (mean: 80.30 U/ml compared with 116.35 U/ml) (P = 0 .009), but not of IL-6 (mean: 11.34 pg/l compared with 9.47 pg/l) (P = 0.436). A correlation was found between the duration of asthma and th e severity of the LAR expressed as area under the curve (AUCLAR) (r = 0.50; P < 0.040). Furthermore, a correlation was detected between the level of total IgE and the level of ECP (r = 0.51; P < 0.030). The dec rease in FEV1 during the LAR tended to correlate with the increase of IL-2R (r = 0.48; P = 0.050). This tendency was not found with the incr ease of eosinophils, nor with the increase of ECP. We conclude that bo th lymphocytes and eosinophils are activated by an allergen challenge, but that only the activation of lymphocytes tends to correlate with t he LAR, suggesting that lymphocytes are also closely involved in the p athogenesis of the allergen-induced LAR.