Bacterial Lipoteichoic Acid Induces Capsular Contracture by Activating Innate Immune Response

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.

The authors 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 and eosin, Masson trichrome, and immunohistochemical staining. The expression of cytokines was measured by quantitative reverse transcription polymerase chain reaction. The authors also used pharmacological methods to verify the roles of macrophages and toll-like receptor 2 (TLR2) signaling in this pathological process.

The authors discovered that repeated LTA injection, at a low concentration, could induce thickening of the capsule tissue. Macrophage infiltration and TLR2/nuclear factor-κB signaling activated in this process could be suppressed by macrophage depletion or TLR2 receptor inhibition.

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 can activate capsular contracture.

This finding is of significant importance for understanding that chronic or repeated subclinical infection could activate a persistent immune response and capsular contracture, and provides novel strategies to interfere with the formation of capsular contracture.