Jon M. Hanifin, Janet L. Rogge, Richard H. Bauman
DOI: 10.2340/00015555925256

We previously reported depressed polymorphonuclear leukocyte and monocyte chemotaxis in patients with severe atopic dermatitis. The degree of impairment roughly correlated with the disease severity and chemotaxis was noted to improve rapidly with clinical remissions. This rapid improvement suggested the presence of a short-lived plasma inhibitor of leukocyte function. We used a radio­labeled PMN chemotaxis assay to assess plasma effect on migration. PMN’s were incubated in plasmas from patients with varying degrees of atopic dermatitis then washed and assessed for migration toward endotoxin-stimulated serum attractant. lnhibitory effect varied widely and correlated directly with clinical extent and severity of dermatitis. Serial studies on individual patients showed lessening of plasma inhibitory activity during remissions. PMN’s from patients with atopic dermatitis showed improved migration after incubation in normal plasma. There was no evidence for circulating chemoattractants nor chemotactic factor inactivators. There appears to be a circulating inhibitor of chemotaxis present in plasma during acute flares of atopic dermatitis; the molecular nature of the inhibitor remains to be elucidated.