Bacterial lipoteichoic acid induces capsular contracture by activating innate immune response.

BACKGROUND:Capsular contracture is attributed to an exaggerated fibrosis response within the capsule and is partly associated with bacterial contamination in situ. However, the cellular mechanisms that initiate this response are unclear. METHODS:We developed a mouse model of capsular contracture by repeated injection of 10 μg/ml lipoteichoic acid (LTA). The histological changes in the capsule tissue were measured by hematoxylin-eosin, Masson, and immunohistochemical staining. The expression of cytokines was measured by quantitative reverse-transcription polymerase chain reaction. We also used pharmacological methods to verify the roles of macrophages and Toll-like receptor 2 (TLR2) signaling in this pathological process. RESULTS:We discovered that repeated LTA injection, at a low concentration, could induce the thickening of the capsule tissue. Macrophage infiltration and TLR2/nuclear factor-kappa B (NF-κB) signaling activated in this process could be suppressed by macrophage depletion or TLR2 receptor inhibition. CONCLUSIONS:As TLR2 signal activation was found to cause capsular contracture by inducing macrophage infiltration as a consequence of trace amounts of LTA contamination in situ, this target is helpful for understanding that chronic or repeated subclinical infection could activate capsular contracture.