Setsuko Ito

Early sensitization to house dust mite is a major risk factor for subsequent development of bronchial asthma in Japanese infants with atopic dermatitis: results of a 4-year followup study

BACKGROUND Bronchial asthma (BA) often develops in children with atopic dermatitis (AD). Identification of factors that could predict the development of asthma in children with AD is useful for early intervention. OBJECTIVE We undertook a 4-year followup study to clarify the factors involved in the development of BA in infants with AD. METHODS We registered 169 infants with AD who were free of BA at registration and examined the prevalence and characteristics of the subsequent development of BA among these patients. RESULTS Among the patients followed for 4 years, approximately 45% experienced asthma-like respiratory symptoms, and 35% were diagnosed as asthmatic patients by pediatric allergologists. Patients who developed BA showed early appearance of house dust mite (HDM)-specific immunoglobulin E (IgE) and persistently high levels of food-specific IgE. Male sex, a positive family history of BA, and the appearance of HDM-specific IgE were identified as significant risk factors for the early development of BA, but the significance of these parameters decreased thereafter. A positive family history of AD, the outcome of skin lesions, and keeping furred pets were also identified as risk factors in a part of the followup period. Among the parameters examined, the early appearance of HDM-specific IgE was the most significant risk factor. CONCLUSION Appearance of HDM-specific IgE antibodies in early childhood, which seems to be mainly influenced by genetic factors, is a major risk factor for the subsequent development of BA in children with AD, but the influence decreases after longer followup.

IgE receptor-bearing lymphocytes in allergic and nonallergic children.

ABSTRACT: Using a monoclonal anti-human IgE receptor (FceR) antibody, the percentage of FceR(+) cells among peripheral blood lymphocytes in children with or without allergic disorders was determined. The percentage of FctR(+) cells in 63 nonallergic children was 4.3 ± 1.5%, which did not vary with age and was equal to that of adults (4.2 ± 1.2%). Allergic younger children (0–2 yr) showed a significantly higher percentage of FceR(+) cells (7.7 ± 3.0%) than nonallergic younger children (0–2 yr) (4.0 ± 1.3%, p < 0.001). Similarly, in allergic younger children, serum IgE levels (geometric mean = 58.9 IU/ml) were also significantly higher than those of nonallergic younger children (geometric mean = 2.0 IU/ml) (p < 0.01). A positive correlation between the percentages of FccR(+) cells and serum IgE levels was observed (Spearman rank = 0.88, p < 0.01)) in eight allergic younger children (0–2 yr) with serum IgE levels higher than 100 IU/ml. The increase in the percentage of FctR(+) cells in allergic younger children (0–2 yr) was not a secondary phenomenon caused by serum IgE because serum IgE levels in these children were much lower than the concentration at which IgE enhance FceR expression on lymphocytes. In conclusion, FceR(+) lymphocytes may play a regulatory role in IgE synthesis in allergic younger children (0–2 yr).

EFFECTS OF ADENOSINE AND ITS ANALOGUES ON ACTIN POLYMERIZATION IN HUMAN POLYMORPHONUCLEAR LEUCOCYTES

1. The effects of adenosine and its analogues on actin polymerization in human polymorphonuclear leucocytes (PMN) induced by three different chemotactic stimulants, platelet‐activating factor (PAF), N‐formyl‐methionyl‐leucyl‐phenylalanine (FMLP) and an activated fragment of C5 (C5a) were investigated.

The effect of adenosine on the fluorescence responses of chlorotetracycline-loaded human polymorphonuclear leukocytes

Chlorotetracycline has been used in human polymorphonuclear leukocytes as a probe to investigate the state of membrane‐bound calcium. We examined the effect of adenosine on the fluorescence responses of CTC‐loaded PMNs stimulated with the synthetic chemotactic peptide, formylmethionyl‐leucyl‐phenylalanine. Adenosine inhibited the decrease in CTC fluorescence in a dose‐dependent fashion and its effect was reversed by theophylline, an adenosine receptor antagonist. Removal of extracellular adenosine by incubating PMNs with adenosine deaminase abolished the effect of adenosine. These data suggest that adenosine inhibits the release of membrane‐bound calcium in PMNs that normally occurs in response to chemotactic stimuli, acting via PMN surface adenosine receptors.