Expression of interleukin-8 and intercellular cell adhesion molecule-1 in the synovial membrane and cranial cruciate ligament of dogs after rupture of the ligament

Abstract

This cross-sectional clinical study compared inflammation, including expression of the chemokine interleukin (IL)-8 and intercellular cell adhesion molecule-1 (ICAM-1), in the stifle joints of 4 control dogs and 23 dogs with cranial cruciate ligament rupture (CCLR). The CCL, synovial membrane, meniscus, cartilage, and synovial fluid from the affected stifle joints of all the dogs were examined. Inflammatory cell counts were performed on the synovial fluid, and the tissues were processed for histologic study and immunohistochemical detection of IL-8 and ICAM-1. The synovial fluid from the stifle joints of the dogs with CCLR had an increased percentage of neutrophils (P = 0.054) and a decreased percentage of lymphocytes (P = 0.004) but not macrophages compared with the fluid from the control dogs. There was accumulation of inflammatory cells and increased expression of IL-8 and ICAM-1 in the vascular endothelium of the synovial membrane and the CCL of the dogs with CCLR. The increase in inflammatory cells in the stifle joints of dogs with CCLR may therefore be due to increased expression of IL-8 and ICAM-1 in the synovial membrane and the CCL after the injury. These data may help in understanding the mechanisms of inflammation associated with CCLR.

Figure 1

Differential leukocyte counts in smears of synovial fluid from dogs with cranial cruciate ligament rupture (CCLR) and control dogs. Compared with the control smears, the smears from dogs with CCLR showed a greater percentage of neutrophils (A, P = 0.054), a similar percentage of macrophages (B, P = 0.080), and a significantly lower percentage of lymphocytes (C, P = 0.004). Lines indicate median and interquartile range. Asterisk indicates a significant difference.

Figure 2

No inflammation was observed in the synovial membrane (A) and CCL (C) from the control dogs, whereas there were accumulations of inflammatory cells (arrows) in the synovium (B) and the CCL (D) of dogs with CCLR. Hematoxylin and eosin; original magnifications ×400; Inset ×1000.

Figure 3

No staining for interleukin (IL)-8 or intercellular cell adhesion molecule-1 (ICAM-1) was detected in the synovial membrane (A and C, respectively) or the CCL (E and G, respectively) of the control dogs, whereas staining (arrows) for IL-8 and ICAM-1 was seen in the synovium (B and D, respectively) and the CCL (F and H, respectively) of dogs with CCLR, mainly in vascular endothelial cells. Original magnifications ×400.

Figure 4

Omission of the primary antibody resulted in no staining (A), whereas use of a von Willebrand antibody instead of the primary antibody resulted in staining of the vascular endothelial cells of the synovium (B, arrow). Original magnifications ×400.