Role of T Lymphocytes in Experimental Staphylococcus aureus Arthritis

Abstract

Using a recently developed murine model of haematogenously induced Staphylococcus aureus, the authors have characterized the phenotypes and functional properties of inflammatory cells present in the synovium of arthritic mice. The results show that large numbers of granulocytes and macrophages were observed in the inflamed synovia within 24 h of inoculation of S. aureus strain LS-1. Many of the synovial macrophage-like cells strained for cytoplasmic IL-1 alpha and TNF-alpha. Subsequently (> or = 48 h later), a prominent infiltration of T lymphocytes, predominantly of CD4+ phenotype, was observed. Some of the T lymphocytes stained for IL-2 receptor and intracytoplasmic interferon-gamma (IFN-gamma). Surprisingly, in spite of the severe inflammatory process, very few cells expressed MHC class-II molecules in the arthritic synovia. In addition, in vivo depletion of CD4+ T-cells resulted in a considerably milder course of staphylococcal arthritis. The similarities in the phenotype expression of synovial cells and central role of T-cells in S. aureus arthritis as well as in non-infectious models of arthritis, indicate that the process governing joint destruction is likely to be the same, irrespective of the initial stimulus.

Protective role of NK1.1+ cells in experimentalStaphylococcus aureusarthritis

“…Earlier studies have demonstrated the pivotal role of CD4 þ T cells in the progression of septic arthritis [8,9]. In the light of a recent report demonstrating that NK cells can play an important role in down-regulating Th1-mediated experimental colitis by controlling the responses of effector T cells to gut bacteria [28], we analysed the effect of in vivo NK cell depletion on T celldependent inflammation.…”

“…The role of lymphocytes in disease development has been extensively studied. Abdelnour et al have shown that T lymphocytes play a major pathogenic role in the disease [8,9]. Also, B lymphocytes contribute to arthritis, as shown in studies demonstrating that B cell-deficient Xid mice display a less severe arthritis [10].…”

Inhibition of nitric oxide synthase (NOS) aggravates Staphylococcus aureus septicaemia and septic arthritis

“…This could be due to the down-regulation of polyclonal B cell activation as well as T cell activities [41,42]. In this context, B [30] and T cells [3,4] contribute to the progression of septic arthritis. Such effects were, however, not observed when naive (i.e.…”

“…05). In order to check the efficiency of L-NMMA in inhibiting NO synthase, the serum levels of NO 3 ¹ , a stable metabolite of NO, were determined and proved to be significantly decreased in mice treated with L-NMMA compared with controls (70 . 1 Ϯ 7 .…”

“…Using this model we have demonstrated that the host immune response is responsible for most of the sequels as a consequence of infection. More specifically, CD4 T lymphocytes contribute to the disease, since depletion of either CD4 T cells [3] or ab T cell receptor (TCR)-expressing cells [4] ameliorates the disease outcome. The activation and clonal in situ expansion of T cells [3,5] is due to superantigenic properties of the exotoxins produced by S. aureus [6].…”