脂磷壁酸
TLR2型
先天免疫系统
医学
渗透(HVAC)
胶囊
纤维化
挛缩
H&E染色
病理
免疫系统
免疫学
免疫组织化学
生物
细菌
外科
物理
植物
遗传学
金黄色葡萄球菌
热力学
作者
Ikram Ahmad,Tianfan Xuan,Yan Wang,Simin Zhang,Lu Wang,Jianying Gu,Fazhi Qi,Wenjie Luan
标识
DOI:10.1097/prs.0000000000011054
摘要
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.
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