title: Atopic dermatitis: influence of bacterial infections on human monocyte and neutrophil granulocyte functional activities.
abstract: In 15 patients with atopic dermatitis (AD) and without concomitant viral or bacterial infections, chemotaxis, superoxide-anion (O2-) generation, and beta-glucuronidase release of purified monocytes (MO) and neutrophils (PMN) were determined. Defined receptor-dependent stimulators (i.e., N-formyl-methionyl-leucyl-phenylalanine, C5a, and leukotriene B4, as well as native and opsonized zymosan particles) were used for phagocyte stimulation. PMN functional activities in response to the stimuli tested were found to be normal in patients with AD and without infections. MO from these patients revealed a slight enhancement of O2- production after stimulation with opsonized zymosan and a small increase of N-formyl-methionyl-leucyl-phenylalanine-induced chemotaxis. Other MO functions tested were within the normal range. However, investigations of MO and PMN functions during the course of concomitant bacterial infections of three patients with AD demonstrated striking alterations of cellular responsiveness. These changes ranged from enhanced to decreased phagocyte functions, depending on the activity of the infectious disorder. Chemotaxis of PMN and MO was depressed around the third day after onset of the infectious disease. In the beginning of infection, there was a decreased O2- generation and beta-glucuronidase release in PMNs. In MOs, both parameters were enhanced. The results of these investigations provide evidence that functional abnormalities of phagocytes observed in patients with AD are sequelae of concomitant skin infections and not signs of an intrinsic defect present in MOs and PMNs.
authors.affiliation: Department of Dermatology, University of Kiel, West Germany.
authors.forename: U
authors.initials: U
authors.lastname: Mrowietz
authors.forename: U
authors.initials: U
authors.lastname: Konter
authors.forename: R
authors.initials: R
authors.lastname: Traut
authors.forename: J M
authors.initials: JM
authors.lastname: Schröder
authors.forename: E
authors.initials: E
authors.lastname: Christophers
mesh_terms: D000293:Adolescent; D000328:Adult; D001424:Bacterial Infections / Q000097:blood*; D002634:Chemotaxis, Leukocyte; D003182:Complement C5; D015936:Complement C5a; D003876:Dermatitis, Atopic / Q000097:blood*; D005260:Female; D005500:Follow-Up Studies; D005966:Glucuronidase / Q000378:metabolism; D006801:Humans; D007073:Immunoglobulin E / Q000032:analysis; D007975:Leukotriene B4; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000201:enzymology / Q000378:metabolism / Q000502:physiology*; D009240:N-Formylmethionine Leucyl-Phenylalanine; D009504:Neutrophils / Q000201:enzymology / Q000378:metabolism / Q000502:physiology*; D010587:Phagocytosis; D013481:Superoxides / Q000096:biosynthesis
chemical_list: D003182:Complement C5; D013481:Superoxides; D007975:Leukotriene B4; D007073:Immunoglobulin E; D009240:N-Formylmethionine Leucyl-Phenylalanine; D015936:Complement C5a; D005966:Glucuronidase