SESSION TITLE: Cytokines/Cellular Interactions Posters
SESSION TYPE: Original Investigation Poster
PRESENTED ON: Wednesday, October 30, 2013 at 01:30 PM - 02:30 PM
PURPOSE: Bleomycin induced lung injury in adult rats increases expression of interleukin (IL)-1β in central integrative respiratory control structures including the nuclei tractus solitarii (nTS) and area postrema (AP) at 48 hours (h) post-injury. These changes are associated with physiologically significant alterations in ventilatory pattern variability. Notably, breathing pattern continues to be altered even up to 7 days (d). It is unknown if brainstem inflammation persists beyond 48h.
METHODS: Intra-tracheal instillation of bleomycin (3.0U) or saline was performed on adult Sprague-Dawley rats (N=6). Animals were transcardially perfused after 7d with sodium phosphate buffer (PBS) and fixed with paraformaldehyde (PFA) 4%. Brainstems were removed and post-fixed in PFA 4%, cryoprotected in 30% sucrose, and embedded in a tissue freezing medium. Brainstems were cut into sections (20 μm) using a cryostat on a series of duplicate slides and stored at -20°C. Each slide was stained immunohistochemically for IL-1β. Sections were photographed in the area of interest at the same light intensity and exposure time; white balance was performed using imaging software. Staining intensity was assessed in anatomically equivalent sections.
RESULTS: Significant increase in IL-1β immunoreactivity was observed at 7d following lung injury with bleomycin. This was noted in the medullary nTS, AP, and dorsal motor nucleus of the vagus (DMV).
CONCLUSIONS: Brainstem IL-1β expression is markedly increased following bleomycin-induced lung injury at 48h and this effect persists to 7d post-injury. Staining was observed in several key centers of sensory integration and breathing control including the nTS, AP, and DMV.
CLINICAL IMPLICATIONS: IL-1β is clearly present in the brainstem after lung injury and during the period when physiologic changes in breathing occur. Expression is specific to medullary structures that integrate input and output for the respiratory central pattern generator. These data add to growing evidence that central cytokine upregulation may play an important role in modulating the physiologic response to lung inflammation and injury.
DISCLOSURE: The following authors have nothing to disclose: Scott Denstaedt, David Litvin, Yee-hsee Hsieh, David Nethery, Thomas Dick, Christopher Wilson, Frank Jacono
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