Multiple bacteria contribute to intraplaque T-cell activation in atherosclerosis

Infection with microorganisms is considered a pathogenic factor in atherogenesis. Several studies have shown the presence of a broad spectrum of bacterial species in atherosclerotic plaques, which could trigger local inflammation. Because T cells contribute to atherosclerotic plaque inflammation, we studied the responsiveness of human plaque derived T-cell cultures to bacteria of different species.

Primary polyclonal T-cell cultures were generated from both carotid endarterectomy tissue and peripheral blood of nine patients, and the peripheral blood of eight matched controls. The in vitro proliferative responses of the T-cell cultures against H. pylori, N. meningitidis, N. lactamica, S. aureus, S. pneumoniae, S. epidermidis and E. coli were analysed. T-cell proliferation was measured by (3)H-thymidine incorporation and expressed as a stimulation index. Selective outgrowth of intraplaque microbial specific T cells was studied by calculating the ratio of plaque T-cell SI and peripheral blood T-cell SI in each patient.

All patients showed T-cell responsiveness to multiple bacteria in their plaque tissue. Stimulation indices were in the range of 0.3-30, and this degree of reactivity with the different species was heterogeneous among patients. Selective outgrowth (plaque/peripheral blood ratio) of T cells against multiple bacteria was observed in six out of nine patients.

T cells in atherosclerotic plaques have the capacity to selectively respond to antigens of a wide variety of microbial antigens. This supports the view that such mechanisms could contribute to the atherosclerotic inflammatory response.