Abstract

BackgroundInflammatory response has been proven to play a crucial role in the pathophysilogical process after traumatic brain injury (TBI). Myeloid differentiation primary response protein 88 (Myd88) is considered as a vital factor for inflammation and immunity. Therefore, it is essential to know the detailed expression of Myd88 after TBI. However, the expression patterns of Myd88 in patients with TBI remain obscure. Hence, the aim of present study was to investigate the cortical expression of Myd88 in human contused brain. MethodsNineteen contused brain tissue biopsies were obtained from 19 patients undergoing surgery for brain contusions 3 h–17 d after trauma, and samples of control group were from three patients in the pathway during surgical removal of deep benign tumors. The expression of Myd88 was assessed by quantitative real-time polymerase chain reaction, Western blotting, immunohistochemistry and double immunofluorescent staining, and the messenger RNA (mRNA) levels of tumor necrosis factor-alpha (TNF-α) and interleukin 1beta (IL-1β) were measured by quantitative real-time polymerase chain reaction. ResultsThe progressively elevated mRNA and protein levels of Myd88 were detected after trauma, with the maximum after 72 h post-injury, and the distribution of Myd88 was found in neurons, astrocytes, and microglia. TNF-α and IL-1β mRNA levels ascended significantly within 12 h, and then descended gradually until after 72 h post-injury. Interestingly, there was a positive relationship between the expression of Myd88 and the proinflammatory cytokine TNF-α. ConclusionsThese findings indicated that Myd88 might play an important role in the inflammatory response after human TBI.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.