Abstract
Two cases of Hyper IgE syndrome were studied immunologically and the following results were obtained.
(1) The cellular immunity and NBT-dye reduction tests were revealed normal. One of the 2 cases showed normal phagocytosis-bacteriocidal activity of polymorphonuclear leukocytes (PMN) using clinically isolated staphylococcus aureus.
(2) Chemotaxis of PMN were depressed or normal inaccordant with the levels of the total serum IgE or the titers of anti-staphylococcal IgE antibody or the existence of skin pustules.
(3) H2 sensitivity of PMN was frequently revealed to be low compared with normal controls. This H2 hyposensitivity was suspected due to the tachyphylaxis of histamine because of the exposure of PMN to the histamine released in vivo.
(4) The titers of anti-staphylococcal IgE antibody were high and booster effect was suspected. Anti-staphylococcal agglutination titers were normal in the 2 cases.
These results suggested that the susceptibility of this syndrome to the infection of staphylococcus aureus could not be explained by only the depression of chemotaxis of PMN.
It was considered that the chemical mediators were released from the anti-staphylococcal IgE antibody bearing mast cells which reacted to the organisms. These chemical mediators included histamine but PMN of H2 hyposensitivity could not be controlled by histamine and continued to release lysosomal enzymes.
Then the inflammation was prolonged and the infected tissues became fragile. After all, the infection of staphylococcus aureus was prolonged.
In other words, we could explain the susceptibility to the infection of staphylococcus aureus by so-called infectious allergy.
