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Roles of neutrophil‐mediated inflammatory response in the bony repair of injured growth plate cartilage in young rats
Author(s) -
Chung Rosa,
Cool Johanna C.,
Scherer Michaela A.,
Foster Bruce K.,
Xian Cory J.
Publication year - 2006
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.0606365
Subject(s) - chondrogenesis , mesenchymal stem cell , cartilage , chemokine , infiltration (hvac) , biology , immunology , cartilage oligomeric matrix protein , proinflammatory cytokine , inflammation , microbiology and biotechnology , medicine , pathology , anatomy , materials science , osteoarthritis , alternative medicine , composite material
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 neutrophils 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 neutrophil chemotactic chemokine cytokine‐induced neutrophil chemoattractant‐1 and cytokines TNF‐α and IL‐1β. 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‐α and IL‐1β and growth factors, platelet‐derived growth factor‐B and TGF‐β1, 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‐α1 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.