We generated > 10⁷ mast cells by culturing 10⁷ cord blood mononuclear cells for > 10 weeks in the presence of Steel factor, interleukin-6 and prostaglandin E₂. 99% of the cultured cells had tryptase-positive granules, while 18% had chymase-positive granules. Cultured mast cells contained 3.6 μg histamine and 3.5 μg tryptase per 10⁶ cells. Cells sensitized with 1 μg/ml human IgE released 58.5% histamine and 1.55 ng tumor necrosis factor (TNF)-α per 10⁶ cells when challenged with 1 μg/ml antihuman IgE, whereas the control cells spontaneously released 3.7% histamine and 0.18ng TNF-α. Analysis for surface antigens revealed that cultured mast cells expressed the following CD molecules: 9, 13, 14, 29, 33, 38, 43, 44, 45RA, 45RB, 46, 47, 48, 49d, 50, 51, 53, 54, 55, 58, 59, 60, 61 and 117 (c-Kit). Taken together, these cultured cells seem to be functionally mature mast cells.

We examined the effect of ATP and related nucleotides on the changes in intracellular calcium ([Ca²⁺]_i) in murine bone marrow-derived mast cells (BMMC) and human cord blood-derived eosinophils (EO) cultured in the presence of interleukins. ATP, ADP and AMP released a substantial amount of histamine and leukotriene C4 from BMMC, and EO showed locomotive activity in response to ATP, ADP and GTP. These reactions were accompanied with an increase in [Ca²⁺]_i in BMMC and in EO. The rise in [Ca²⁺]_i in BMMC induced by ATP or antigen at optimal concentrations was inclined to be persisting. On the other hand, these nucleotides induced a rapid and transient rise in [Ca²⁺]_i in EO. Purified human peripheral EO also exhibited locomotive activity and an increase in [Ca²⁺]_i in response to ATP. These results indicate that extracellular ATP activates interleukin-dependent cultured mast cells and EO through Ca²⁺ mobilization, and suggest that ATP, which is known to be released from activated platelets or autonomic nerves, may stimulate in vivo counterparts of these cultured inflammatory cells.

We studied the l-type isoproterenol inhalation therapy for patients with severe asthmatic attacks who were admitted at the Department of Allergy of National Children’s Hospital from 1981 to 1991. One hour after l-type isoproterenol inhalation therapy, statistically significant effects were noted with regard to the asthmatic status. Moreover, no side effect was found amoung the subjects. From these data, l-type isoproterenol inhalation therapy is thought to be effective for severe asthmatic attacks.

The incidence of latex-induced allergy has been reported to be increasing in Europe and the US but not in Japan. We thus measured latex-specific IgE antibodies and latex-specific IgG antibodies in sera from 196 atopic children with low serum IgE levels (under 1,000 U/ml; group 1), 108 atopic children with high serum IgE levels (over 1,000 U/ml; group 2) and 601 hospital employees (group 3). Atopic children were diagnosed as having asthma, atopic dermatitis and/or food intolerance. One out of group 1 (0.5%) and 11 out of group 2 (10.2%) were found to have latex-specific IgE by radioallergosorbent assay (RAST), and 7 were further found to be positive for latex antigen by skin test. Fifty-five percent of group 1, 65% of group 2 and 9.7% of group 3 were found to have latex-specific IgG over 100 units/ml by enzyme linked immunosorbent assay (ELISA). Prior to our diagnosis most of the children and employees did not realize they were allergic to latex. These data suggest that caution should be taken regarding latex allergy when atopic children have to be operated upon as atopic children tend to be sensitized to the latex antigen after even minimal contact with latex products.

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