Macrophages and other cells of the innate immune system recognize foreign particles that could be potentially dangerous and respond by initiating an inflammatory response. The biologically active chemical mediators of this response called pro-inflammatory cytokines are produced in various myeloid derived immune cells and can affect other cells of the body. Interleukin-1β, a pro-inflammatory cytokine, has been shown to have direct effects on dorsal root ganglion (DRG) cell bodies including the upregulation and direct release of a nociceptive neurotransmitter called substance P (SP). Using a zymosan-induced model of systemic inflammation, we hypothesized that murine DRG neurons and the nerve processes associated with them in the dorsal horn of the spinal cord (SC) at the L1 level will show an upregulation of SP expression in response to inflammation in the peritoneum. Experimental mice were treated with a zymosan suspension (500mg/kg, intraperitoneal injection), and control mice received sterile filtered solution (intraperitoneal injection). Both DRG and SC specimens were collected after in situ fixation and subjected to immunofluorescence staining to label SP. Using confocal microscopy, fluorescence microscopy, and image analysis software this expression of SP was quantified and compared. In both tissue specimen groups, an increase in SP expression was discovered in zymosan treated mice. The exact cause of this increase was not specifically determined in this experiment. This experiment provided valuable insight about how a systemic inflammatory response can affect sensory nerve function. Successful methods for further experimentation were identified and information about the zymosan model of inflammation was obtained
Identifer | oai:union.ndltd.org:ETSU/oai:dc.etsu.edu:honors-1356 |
Date | 01 May 2016 |
Creators | Armstrong, Michael G |
Publisher | Digital Commons @ East Tennessee State University |
Source Sets | East Tennessee State University |
Detected Language | English |
Type | text |
Format | application/pdf |
Source | Undergraduate Honors Theses |
Rights | Copyright by the authors., http://creativecommons.org/licenses/by-nc-nd/3.0/ |
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