scholarly journals Distribution of Bone Marrow-Derived Cells in the Fracture Callus during Plate Fixation in a Green Fluorescent Protein-Chimeric Mouse Model

2011 ◽  
Vol 60 (5) ◽  
pp. 455-462 ◽  
Author(s):  
Masaki UENO ◽  
Kentaro UCHIDA ◽  
Masashi TAKASO ◽  
Hiroaki MINEHARA ◽  
Kaori SUTO ◽  
...  
2016 ◽  
Vol 42 (2) ◽  
pp. 263-268 ◽  
Author(s):  
Wenan Xu ◽  
Shan Jiang ◽  
Qiuyue Chen ◽  
Yanyan Ye ◽  
Jiajing Chen ◽  
...  

2016 ◽  
Vol 17 (3) ◽  
pp. 280-290 ◽  
Author(s):  
B. R. Achyut ◽  
Adarsh Shankar ◽  
A. S. M. Iskander ◽  
Roxan Ara ◽  
Robert A. Knight ◽  
...  

2008 ◽  
Vol 22 (S2) ◽  
pp. 67-67
Author(s):  
Lydia S. Glaw ◽  
James A. Thomas ◽  
Dominique L. Thacker ◽  
Gary K. Owens ◽  
Thomas C. Skalak

2009 ◽  
Vol 1 ◽  
pp. OED.S2813 ◽  
Author(s):  
Jared E. Knickelbein ◽  
Simon C. Watkins ◽  
Paul G. Mcmenamin ◽  
Robert L. Hendricks

The composition and location of professional antigen presenting cells (APC) varies in different mucosal surfaces. The cornea, long considered an immune-privileged tissue devoid of APCs, is now known to host a heterogeneous network of bone marrow-derived cells. Here, we utilized transgenic mice that express enhanced green fluorescent protein (EGFP) from the CD 11c promoter (pCD11c) in conjunction with immunohistochemical staining to demonstrate an interesting stratification of APCs within non-inflamed murine corneas. pCD11c+ dendritic cells (DCs) reside in the basal epithelium, seemingly embedded in the basement membrane. Most DCs express MHC class II on at least some dendrites, which extend up to 50 μm in length and traverse up 20 μm tangentially towards the apical surface of the epithelium. The DC density diminishes from peripheral to central cornea. Beneath the DCs and adjacent to the stromal side of the basement membrane reside pCD11c–CD11b+ putative macrophages that express low levels of MHC class II. Finally, MHC class II–pCD11c–CD11b+ cells form a network throughout the remainder of the stroma. This highly reproducible stratification of bone marrow-derived cells is suggestive of a progression from an APC function at the exposed corneal surface to an innate immune barrier function deeper in the stroma.


2020 ◽  
Vol 9 (2) ◽  
pp. 71-76
Author(s):  
Tao Gao ◽  
Junqing Lin ◽  
Changqing Zhang ◽  
Hongyi Zhu ◽  
Xianyou Zheng

Aims The purpose of this study was to determine whether intracellular Staphylococcus aureus is associated with recurrent infection in a rat model of open fracture. Methods After stabilizing with Kirschner wire, we created a midshaft femur fracture in Sprague-Dawley rats and infected the wound with green fluorescent protein (GFP)-tagged S. aureus. After repeated debridement and negative swab culture was achieved, the isolation of GFP-containing cells from skin, bone marrow, and muscle was then performed. The composition and viability of intracellular S. aureus in isolated GFP-positive cells was assessed. We suppressed the host immune system and observed whether recurrent infection would occur. Finally, rats were assigned to one of six treatment groups (a combination of antibiotic treatment and implant removal/retention). The proportion of successful eradication was determined. Results Green fluorescent protein-containing cells were successfully isolated after the swab culture was negative from skin (n = 0, 0%), muscle (n = 10, 100%), and bone marrow (n = 10, 100%) of a total of ten rats. The phagocytes were predominant in GFP-positive cells from muscle (73%) and bone marrow (81%) with a significantly higher viability of intracellular S. aureus (all p-values < 0.001). The recurrent infection occurred in up to 75% of rats after the immunosuppression. The proportion of successful eradication was not associated with implant retention or removal, and the efficacy of linezolid in eradicating intracellular S. aureus is significantly higher than that of vancomycin. Conclusion Intracellular S. aureus is associated with recurrent infection in the rat model of open fracture. Usage of linezolid, a membrane-permeable antibiotic, is an effective strategy against intracellular S. aureus. Cite this article: Bone Joint Res. 2020;9(2):71–76.


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