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Patterns of acute inflammatory response to cell transplantation surgery at the graft site
EANS Academy. Abdulla M. Sep 27, 2019; 276067; EP11009
Mutwakil Abdulla
Mutwakil Abdulla

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Abstract
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Objective: Achieving good graft survival is a key issue for cell transplantation in the brain. Most cell death occurs early after surgery due to poorly defined mechanisms. Here, we probe cellular and molecular inflammatory response to surgical trauma at the graft site in a Huntington's Disease (HD) transgenic mouse model.
Subjects: 52 Q175 (HD-Tr), and 52 Wild-type mice (Wt).
Design: All mice underwent unilateral stereotactic needle injury to the striatum. Mice were sacrificed 1 hour, 72 hours and 1 week after surgery (32 Tr and 32 Wt for histology, and 20 Tr and 20 Wt for molecular analysis).
Methods: For cell studies: Brain sections were stained with Iba-1 antibody. Cells positive for Iba-1 were quantified using stereological methods.
For molecular studies: 3mm cubes of brain tissue centred on the needle tract were dissected and tested for 29 different cytokines/chemokines using a multiplex system. Corresponding samples from contralateral hemispheres and from non-injured animals were used as controls.
Results: Cell studies: Significantly increased numbers of Iba-1 positive cells were observed in Tr mice compared to Wt at baseline. More Iba-1 positive cells were recruited to injury sites 72 hours after surgery than at earlier time points. This recruitment was more noticeable in Tr animals.
Molecular studies: Both Tr and Wt mice exhibited increased levels of IL1B, IL6, KC/GRO and TNFα at the injury site, peaking 1 hour after surgery, compared to matched controls or to the contralateral hemisphere. At 1 hour, Tr animals showed significantly increased levels of IL1B and TNFα compared to Wt. IL6 continued to be detected in significant amounts 24 hours after surgery.
Conclusions: Inflammatory responses to trauma at the graft site could contribute to poor graft survival. The HD brain shows an enhanced response to injury, suggesting that the inflammatory component of neurodegeneration could enhance graft site hostility.
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