S01.3 THE IMMUNE RESPONSE IN PATIENTS WITH IMPLANT-ASSOCIATED OSTEOMYELITIS: EXPRESSION OF TOLL-LIKE RECEPTORS ON PERIPHERAL T CELLS

Abstract

Implant-associated osteomyelitis is caused by persistent bacterial infections, predominantly by staphylococci species forming biofilms on implants or osteosynthesis – materials. In the majority of patients the systemic immune response appears to be inconspicous with only minor upregulation of activation-associated receptors on the polymorphonuclear neutrophils (PMN). We found, however, evidence the activation of T cells, apparent as the expansion of CD4+ and CD8+ T cells bearing the activation-associated receptor CD11b. These cells also lacked the co-stimulatory molecule CD28, which is a further indicator for T cell activation. Moreover, small populations of T cells expressing Toll-like receptors (TLR)1, TLR2 or TLR4 were detected in the patients, while in healthy donors less than 1 % of T cells express TLR. A preferential association of TLR1- and TLR2-expression with CD28-CD11b+ cells was seen, compatible with the fact these cells represent an activated phenotype. In addition to the peripheral blood we also analysed leukocytes recovered from the infected site during surgery for removal of the implant. Predominantly PMN were found, highly activated as judged from their surace recpetor pattern, but also CD4+ and CD8+ T cells. As expected, these T cells represented an activated phenotype, and particularly the CD8+ cells expressed CD57, a receptor identifying end-differentiated T cells. The T cells recovered from the infected site, but not the peripheral blood T cells, produced interferon gamma, a cytokine known to support the function of phagocytic cells. In conclusion our data provide evidence that in response to local, persistent bacterial infections T cells are activated to acquire – among others – receptors selective for bacterial products, which in turn might modulate the T cell function and hence the host defence.