Defective monokine production and decreased responsiveness of polymorphonuclear leukocytes to recombinant interleukin-1 in asthmatic patients.

Augmented IgE production and increased infections are often seen in allergic patients. As monocytes (MN) and polymorphonuclear leukocytes (PMN) are involved in both immune regulation and inflammatory reaction, MN function in terms of monokine production stimulated with lipopolysaccharide (MN supernatant; MN-sup) and its biological activity and the response of PMN to MN-sup and recombinant interleukin-1 (rIL-1) regarding chemotactic activity and expression of IgG Fc receptor (FcR) were studied in 26 normal children and 28 new and 22 hyposensitized (HS) asthmatic children. The results showed the following. There was no difference in IL-1 production, as assayed by thymocyte proliferation, among the three groups. All MN-sup from the three groups could enhance IL-2 production, but that of new patients was less efficient. In the absence of PWM, MN-sup of new patients greatly augmented the production of IgG, IgA, IgM, and IgE, but that of HS patients could enhance only IgE synthesis. MN-sup of patients enhanced less efficiently the chemotactic activity and FcR expression of PMN from healthy volunteers, and PMN from asthmatics responded much less vigorously to rIL-1 regarding the above-mentioned functions. The number of PMN with membrane IL-1 was much lower in allergic patients. Thus the abnormal MN and PMN functions may be used to explain partly the augmented IgE production and increased infections in allergic patients.