When a traumatic skeletal muscle injury occurs, such as crushing, contusion, laceration, or freezing, the body must mount an inflammatory response in order to clear muscle debris and fully regenerate the damaged muscle. This response is made up primarily of an innate immune response, which is amplified by the release of pro-inflammatory cytokines and chemokines and leads to the activation of several specific myeloid cell populations. The neutrophil, the first myeloid cell to infiltrate injured muscle, is attracted by the cytokines IFN-γ and TNF-α and the chemokines CXCL1 and CXCL5. However, the timing and magnitude of CXCL1 and CXCL5 signaling following muscle injury have not been carefully examined. Using a freeze injury model to induce a traumatic injury to muscle and real-time PCR, we showed that CXCL1 and CXCL5 expression is rapidly upregulated, within 60 minutes and 3 hours, respectively, in mouse tibialis anterior (TA) muscles following injury. This finding serves as a starting point in the characterization of pro-inflammatory chemokines’ impacts on the muscle injury inflammatory response.
This research was supported by the Undergraduate Research Opportunities Program (UROP).
Jergenson, Matthew; Le, Gengyun; Lowe, Dawn. A..
Expression of Pro-inflammatory Chemokines CXCL1 and CXCL5 is Rapidly Upregulated Following Traumatic Injury.
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