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Journal of Histochemistry and Cytochemistry, Vol. 45, 1247-1254, Copyright © 1997 by The Histochemical Society, Inc.

ARTICLE

ICAM-1/LFA-1 Expression in Acute Osteodestructive Joint Lesions in Collagen-induced Arthritis in Rats

Matthias F. Seidela,b, Rolf Kecka, and Hans Vetterb
a Institut für angewandte Zellkommunikationsforschung, Bonn, Germany
b Medizinische Poliklinik der Universität Bonn , Bonn, Germany

Correspondence to: Matthias F. Seidel, Medizinische Poliklinik der Universität Bonn, Wilhelmstr. 35-37, D-53111 Bonn, Germany.

Collagen-induced arthritis in rats is a widely used model of rheumatoid arthritis (RA). However, the joint immunohistopathology is less well characterized. The objective of this study was therefore to analyze whole ankle joints for markers known to mediate inflammatory mechanisms in RA. Indirect immunohistochemistry was performed on undecalcified cryostat sections for intercellular adhesion molecule-1 (ICAM-1, clone 1A 29) and leukocyte function-associated antigen-1 (LFA-1, clone WT.1) expression, for CD4+ lymphocytes (clone W3/25), B-cells (clone HIS 14), and macrophages (clone ED2). Acute, osteodestructive arthritis (n = 8) induced with bovine collagen Type II was verified by clinical and radiological measures. LFA-1 expression was found almost exclusively at sites associated with cartilage erosion or osteodestruction. ICAM-1 was similarly expressed in the vicinity of tissue degradation but also by blood vessels in peripheral areas of joint swelling. CD4+ lymphocytes and macrophages were more ubiquitous. B-cells were infrequent. In control animals (n = 4) ICAM-1 was expressed by synovial blood vessels. Macrophages were identified at the synovial lining. The results suggest that LFA-1 and ICAM-1 mediate important inflammatory events in this model. Similar findings in human RA synovium provide further arguments that collagen-induced arthritis in rats might be regarded as a comparable disease. (J Histochem Cytochem 45:1247-1253, 1997)

Key Words: rheumatoid, collagen, rat, arthritis, osteodestruction, immunohistopathology, ICAM-1, LFA-1, CD4


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