Lloyd V. Crawford

Characteristics of diatrizoate-induced basophil histamine release

Factors influencing the release of histamine by basophils exposed to the radiocontrast agent diatrizoate were investigated in vitro by use of cells from healthy adult subjects with no history of radiocontrast reactions. Diatrizoate-induced release shared similarities with calcium ionophore-induced release. The response to both agents is dose dependent, enhanced by deuterium oxide, optimal at 37 degrees C, calcium dependent, and enhanced with longer reaction times. Unlike calcium ionophore, however, pretreatment of basophils with diatrizoate may also induce dose-dependent inhibition of reactivity during subsequent challenges with anti-IgE, N-formyl methionine peptide, and calcium ionophore. These findings suggest that diatrizoate may induce histamine release via a calcium ionophore-like mechanism, but other effects on cellular function probably account for its ability to inhibit basophil responsiveness.

Characterization of mononuclear cell-derived histamine release enhancing factor

Histamine release enhancing factor (HREF) is a product of phytohemagglutinin-stimulated mononuclear cells that substantially augments in vitro IgE-mediated basophil histamine release. The factor is stable at 56 degrees C and has a molecular weight in the 10,000 to 30,000 dalton range. The magnitude of HREF activity produced is dependent on the concentration of mononuclear cells cultured and the final concentration of HREF during basophil challenge. The HREF phenomenon could not be attributed to phytohemagglutinin, alpha- or gamma-interferon, arachidonic acid metabolites, or interleukin-1 or 2. HREF appears to be a unique cytokine of potential importance in the immunology of inflammatory and atopic processes.

1041 REDUCED PRODUCTION OF HISTAMINE RELEASE ENHANCING FACTOR (HREF) BY CORD BLOOD MONONUCLEAR CELLS

The liberation of histamine and other inflammatory mediators constitute a major component of host defense. HREF is a unique cytokine produced by PHA stim. mononuclear cells (MC) that may be an important mediator of inflammatory responses. Incubation of granulocytes with HREF enhanced subsequent basophil histamine release (BHR) induced by anti-IgE, f-Met peptide, and the Ca ionophore A23187 (124±43%, 139±40%, and 66±29% enhancement). HREF production was dependent on the number of cells cultured, PHA cone., and duration of culture. Conditioned media containing HREF was active after heat (70°C × 30 min), absorption by activated lymphocytes, and thyroglobulin removal of PHA. HREF produced by cord blood MC of 19 newborns produced significantly less enhancement of anti-IgE induced BHR than adult controls (39±30% vs 53±31% enhancement, p<.05). This was not related to impaired PHA responsiveness. Both stim. and unstim. cord MC incorporated greater 3H thymidine than controls (p <.001). T cell enriched (TCE) populations produced greater HREF than unfrac. or T-depleted (TD) populations (TCE 73±32% enhancement; unfrac. 42±20%; TD 43±25%; N=13, p <0.05). Functional cellular immune deficiency in newborns and deficient lymphokine synthesis by cord lymphocytes have been previously reported. HREF is a potentially important determinant of histamine release and reduced capacity for its production may contribute to the relative immunodeficiency of newborns.

Treatment of allergic eczema versus seborrheic infantile eczema

Summary In order to control allergic infantile eczema, as well as to diminish the chances of progression to asthma, search for specific excitants by means of hypoallergic diets, environmental control measures, and, at times, allergic skin testing is mandatory. The treatment of choice for pollen eczema is hyposensitization. The symptomatic treatment of allergic eczema is discussed. Since the etiology of seborrheic infantile eczema is unknown, but is not allergic, no specific search for excitants is indicated. The symptomatic treatment of seborrheic eczema is the most important consideration and is discussed.