Adhesion Molecule Expression in Polymorphic Light Eruption

Endothelial leukocyte adhesion molecule-1 (ELAM-1), vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) are cytokine-regulated cell-surface Ieukocyte adhesion molecules. We have investigated the in vivo kinetics and pattern of expression of these adhesion molecules in relation to tissue accumulation of leukocytes in the photodermatosis, polymorphic light eruption (PMLE), which is characterized by dense perivascular leukocytic infiltration. Immunohistology was performed on biopsies taken at varying time points from PMLE lesions induced in 11 subjects by suberythemal solar simulated irradiation. Vascular endothelial ELAM-1 expression was first observed at 5 h, maximal at 24 to 72 h, and remained elevated at 6 d. VCAM-1, minimally expressed in control skin, was induced above background levels on endothelium and some perivascular cells after 24h and maintained at 6 d. Endothelial cell ICAM-1 expression was increased above control levels at 72h and 6 d. Keratinocyte ICAM-1 expression, most marked overlying areas of dermal leukocytic infiltration, began at 5h and was strong at 72h and 6 d. In addition to lymphocytes, significant number of neutrophils of but not eosinophils were detected in the dermal leukocytic infiltrate that appeared at 5h and persisted at 6 d. The pattern of adhesion molecule expression that we have observed is similar to that seen in normal skin during a delayed hypersensitivity reaction: These observations support an immunologic basis for PMLE

Biomarkers of the involvement of mast cells, basophils and eosinophils in asthma and allergic diseases

Biomarkers of disease activity have come into wide use in the study of mechanisms of human disease and in clinical medicine to both diagnose and predict disease course; as well as to monitor response to therapeutic intervention. Here we review biomarkers of the involvement of mast cells, basophils, and eosinophils in human allergic inflammation. Included are surface markers of cell activation as well as specific products of these inflammatory cells that implicate specific cell types in the inflammatory process and are of possible value in clinical research as well as within decisions made in the practice of allergy-immunology

Reflections on eosinophils and flame figures: Where there's smoke there's not necessarily wells syndrome

Eosinophils were first described in 1879 by Paul Ehrlich, who recognized their ability to stain with acid dyes, particularly eosin. The distinctive tinctorial properties of eosinophil granules give these cells a prominence in stained sections that contrasts with their lack of diagnostic power and still undefined role in pathogenesis. Eosinophils may be seen in skin biopsy specimens from patients with various inflammatory and neoplastic disorders, but they are among the diagnostic criteria in a limited number of diseases, including Wells syndrome, angiolymphoid hyperplasia with eosinophilia, and eosinophilic pustulosis.1-2 Eosinophils are associated with pathophysiologic mechanisms that strongly implicate them in the pathogenesis of many cutaneous diseases. Eosinophil involvement has been well documented in cutaneous disorders characterized by swelling,3 particularly chronic urticaria,4 pressure urticaria,5 and episodic angioedema.6 Cutaneous edema was the common clinical thread in the first 4 cases reported by Wells.7 Eosinophils also . . . [Full Text of this Article