INHIBITION OF NEUTROPHIL CHEMOTAXIS IN ASSOCIATION WITH EXPERIMENTAL ANGIOEDEMA IN PATIENTS WITH COLD URTICARIA - A MODEL OF CHEMOTACTIC DEACTIVATION INVIVO

  • 1 January 1979
    • journal article
    • research article
    • Vol. 35  (1) , 112-118
Abstract
Deactivation is a phenomenon in which leukocytes exposed in vitro to a chemotactic factor in the absence of a concentration gradient are rendered relatively unresponsive to stimulation by a subsequent chemotactic gradient. In patients with idiopathic cold-induced urticaria, the elicitation of a local experimental angioedematous lesion causes the release of 2 chemotactic principles which deactivate leukocytes in vitro, high MW neutrophil chemotactic factor (HMW-NCF) and eosinophil chemotactic factor of anaphylaxis (ECF-A), into the venous circulation draining the challenged extremity. Biopsy specimens of lesional skin sites obtained for up to 24 h show no infiltration of cells. For this reason, the in vitro chemotactic responsiveness of neutrophils to the chemotactic factor HMW-NCF and C5 [complement component 5] fragments were assessed in 3 patients at various times after experimental challenge. Leukocytes from the venous effluent draining an experimentally-induced angioedematous lesion were markedly impaired in their chemotactic responsiveness to both chemotactic factors 5 min after challenge, while cells taken from an unchallenged extremity at the same time responded normally. Cells from both arms were equally impaired in their responsiveness 1 h later, demonstrating that the chemotactic defect becomes systemic. The acquired defect was dissipated 4 h after challenge. Deactivation may occur in vivo and may alter host responsiveness in states where chemotactic factors are released into the circulation.

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