Staphylococcus epidermidis infections are usually nosocomial and involve colonization of biomaterials. The immune defense system cannot efficiently control the bacteria during these infections, which often results in protracted chronic inflammation, in which a key event is disturbed removal of neutrophils by tissue macrophages. While ingesting uninfected apoptotic neutrophils, macrophages release anti-inflammatory cytokines that lead to resolution of inflammation. In clinical studies, we have previously found elevated levels of the proinflammatory cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 in synovial fluid from prostheses infected with coagulase negative staphylococci. We show that macrophages phagocytosing apoptotic neutrophils containing S. epidermidis released TNF-alpha and interleukin-6, whereas macrophages phagocytosing spontaneously apoptotic neutrophils did not. This difference was not due to dissimilar phagocytic capacities, because macrophages ingested both types of neutrophils to the same extent. The activation was induced mainly by the apoptotic neutrophils themselves, not by the few remaining extracellular bacteria. Macrophages were not activated by apoptotic neutrophils that contained paraformaldehyde-killed S. epidermidis. Proinflammatory reactions induced by clearance of apoptotic neutrophils containing S. epidermidis might represent an important mechanism to combat the infective agent. This activation of macrophages may contribute to the development of chronic inflammation instead of inflammation resolution.

译文

表皮葡萄球菌感染通常是医院内的,涉及生物材料的定植。在这些感染期间,免疫防御系统无法有效控制细菌,这通常会导致长期的慢性炎症,其中关键事件是组织巨噬细胞干扰中性粒细胞的去除。在摄取未感染的凋亡中性粒细胞时,巨噬细胞会释放抗炎细胞因子,从而缓解炎症。在临床研究中,我们先前已发现感染凝固酶阴性葡萄球菌的假体的滑液中促炎细胞因子肿瘤坏死因子-α (TNF-α) 和interleukin-6水平升高。我们显示巨噬细胞吞噬含有表皮葡萄球菌的凋亡中性粒细胞释放TNF-α 和interleukin-6,而吞噬自发凋亡中性粒细胞的巨噬细胞却没有。这种差异不是由于吞噬能力不同,因为巨噬细胞在相同程度上摄取了两种类型的中性粒细胞。激活主要是由凋亡的中性粒细胞本身诱导的,而不是由少数剩余的细胞外细菌诱导的。巨噬细胞不被含有多聚甲醛杀死的表皮葡萄球菌的凋亡中性粒细胞激活。清除含有表皮葡萄球菌的凋亡中性粒细胞引起的促炎反应可能是对抗感染剂的重要机制。巨噬细胞的这种激活可能有助于慢性炎症的发展,而不是炎症的解决。

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