Involvement of cytokines and vascular adhesion receptors in the pathology of fronto-ethmoidal mucocoeles.
Fronto-ethmoidal mucocoeles have the capacity to destroy bone. Sinus lining tissue has been obtained at surgery from patients with mucocoeles, from those with chronic sinusitis undergoing endoscopic sinus surgery and from patients undergoing craniofacial resection. Tissues have been frozen, sectioned, and subjected to immunohistochemical examination with monospecific antibodies for the presence of the potent osteolytic cytokines interleukins-1 and -6 and tumour necrosis factor alpha. In addition, the chemotactic intercrine--interleukin-8 was investigated. The presence of the cytokine-inducible vascular endothelial adhesion receptors--Inter-Cellular Adhesion Molecule (ICAM)-1 and E-Selectin (also known as Endothelial Leukocyte Adhesion Molecule--ELAM) was also determined. Normal sinus tissue showed no immunoreactivity with the antibodies to these various moieties. Surprisingly, only a small proportion of tissues from patients with chronic sinusitis showed the presence of cytokines or vascular adhesion receptors. In contrast, all specimens of fronto-ethmoidal mucocoeles showed positive staining for IL-1 alpha and beta and for ICAM-1 and E-selectin. IL-1 immunostaining was restricted to the epithelial cell population not being found in infiltrating leukocytes. In 40% of mucocoeles infiltrating macrophage-like cells showed the presence of tumour necrosis factor alpha. The presence of the potent osteolytic cytokine--IL-1 in all specimens of fronto-ethmoidal mucocoeles coupled to the finding of the IL-1-inducible adhesion molecules ICAM-1 and E-Selectin argues strongly that IL-1 is released from the epithelial cells and that this cytokine may be the factor causing the erosion of bone overlying the expanding mucocoele. The nature of the signals inducing cytokine synthesis remain, however, unidentified.
Lund
V J
VJ
Institute of Laryngology and Otology, London, UK.
Henderson
B
B
Song
Y
Y
D000328:Adult; D000368:Aged; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis*; D015815:Cell Adhesion Molecules / Q000032:analysis*; D002630:Chemotactic Factors / Q000032:analysis; D016207:Cytokines / Q000032:analysis*; D019040:E-Selectin; D005005:Ethmoid Sinus / Q000473:pathology*; D005260:Female; D005626:Frontal Sinus / Q000473:pathology*; D006801:Humans; D018799:Intercellular Adhesion Molecule-1; D007375:Interleukin-1 / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D016209:Interleukin-8 / Q000032:analysis; D008264:Macrophages / Q000473:pathology; D008297:Male; D008562:Membrane Glycoproteins / Q000032:analysis; D008875:Middle Aged; D009078:Mucocele / Q000473:pathology*; D009092:Mucous Membrane / Q000473:pathology; D010254:Paranasal Sinus Diseases / Q000473:pathology; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D011971:Receptors, Immunologic / Q000032:analysis; D012852:Sinusitis / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
D015214:Antigens, Differentiation, Myelomonocytic; D015815:Cell Adhesion Molecules; D002630:Chemotactic Factors; D016207:Cytokines; D019040:E-Selectin; D007375:Interleukin-1; D015850:Interleukin-6; D016209:Interleukin-8; D008562:Membrane Glycoproteins; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D011971:Receptors, Immunologic; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1