Roles of neutrophil-mediated inflammatory response in the bony repair of injured growth plate cartilage in young rats
Roles of neutrophil-mediated inflammatory response in the bony repair of injured growth plate cartilage in young rats
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DOI：
10.1189/jlb.0606365
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发表时间：
2006-12-01
影响因子：
5.5
通讯作者：
Xian, Cory J.
中科院分区：
文献类型：
--
作者：
Chung, Rosa;Cool, Johanna C.;Xian, Cory J.
受伤的生长板软骨通常由骨组织修复，导致儿童骨骼生长受损。以前，损伤诱导的初始炎症反应被证明是一种主要含有中性粒细胞的急性炎症事件。为了研究中性粒细胞在骨修复中的潜在作用，在生长板损伤的大鼠中全身给予中性粒细胞中和抗血清或对照正常血清。发现炎症反应与中性粒细胞趋化性趋化因子精氨酸诱导的中性粒细胞趋化因子-1和细胞因子TNF-α和IL-1 β的表达增加在时间上相关。炎症反应后，间充质浸润，软骨和成骨反应，骨修复观察损伤部位。在第1天，在损伤的生长板处，神经元减少没有显著影响其他炎性细胞的浸润以及TNF-α和IL-1 β以及生长因子、血小板衍生生长因子-B和TGF-β 1的表达，并且在第4天对间充质浸润没有影响。然而，到第10天，间充质修复组织的比例显著减少，但骨小梁增加（尽管统计学上不显著），损伤部位内软骨组织减少。结论：在抗血清治疗的大鼠中，成骨细胞分化转录因子cbf-α 1和骨基质蛋白骨钙素的表达增加，软骨形成转录因子Sox-9和软骨基质胶原-II的表达减少。这些结果表明，损伤诱导的，嗜酸性粒细胞介导的炎症反应似乎抑制间充质细胞成骨细胞分化，但增强软骨分化，因此，它可能参与调节下游软骨和成骨事件生长板骨修复。
Injured growth plate cartilage is often repaired by bony tissue, resulting in impaired bone growth in children. Previously, injury-induced, initial inflammatory response was shown to be an acute inflammatory event containing predominantly neutrophils. To examine potential roles of nentrophils in the bony repair, a neutrophil-neutralizing antiserum or control normal serum was administered systemically in rats with growth plate injury. The inflammatory response was found temporally associated with increased expression of nentrophil chemotactic chemokine cytokine-induced nentrophil chemoattractant-1 and cytokines TNF-alpha and IL-1 beta. Following the inflammatory response, mesenchymal infiltration, chondrogenic and osteogenic responses, and bony repair were observed at the injury site. Neutrophil reduction did not significantly affect infiltration of other inflammatory cells and expression of TNF-alpha and IL-1 beta and growth factors, platelet-derived growth factor-B and TGF-beta 1, at the injured growth plate on Day 1 and had no effects on mesenchymal infiltration on Day 4. By Day 10, however, there was a significant reduction in proportion of mesenchymal repair tissue but an increase (although statistically insignificant) in bony trabeculae and a decrease in cartilaginous tissue within the injury site. Consistently, in antiserum-treated rats, there was an increase in expression of osteoblastic differentiation transcription factor cbf-alpha 1 and bone matrix protein osteocalcin and a decrease in chondrogenic transcription factor Sox-9 and cartilage matrix collagen-II in the injured growth plate. These results suggest that injury-induced, neutrophil-mediated inflammatory response appears to suppress mesenchymal cell osteoblastic differentiation but enhance chondrogenic differentiation, and thus, it may be involved in regulating downstream chondrogenic and osteogenic events for growth plate bony repair.