Abstract
The olfactory system has been known to be modulated by a systemic inflammatory stress such as sepsis. The inflammatory stress is intervened by many cytokines such as tumor necrosis factor (TNF)-α. Therefore, the olfactory bulb (OB) which is a major constituent of olfactory system was investigated of its cytokine production as a rapid response to bacterial endotoxin lipopolysaccharide (LPS) and the occurrence of apoptosis as a final event in the OB was also evaluated. Male C3H/HeN mice (eight-week-old; 25-28 g) were injected intraperitoneally with LPS (50 μg/mice) or saline (control). At different time points from 0.5 h to 24 h after the injection the mice were sacrificed and their OB was used for the quantitation of mRNA expression levels by using real-time PCR amplification and the immunohistochemical detection. Peripheral LPS challenge rapidly enhanced the mRNA expression levels in the OB of the genes encoding IκBα, NF-κB, TNF-α and iNOS. The induction of TNF-α mRNA was followed by an increased expression of TNF-α protein. All TNF-α-positive cells, which were mainly present in the granule cell layer or the olfactory nerve layer, were double-labeled with anti-GFAP antibody. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling positive cells were observed in the granule cell layer. These findings provide evidence for rapid OB response to endotoxemia, and suggest that olfactory system may play a role in the modulation of endotoxemia-induced cognitive and behavioral changes. [Jpn J Physiol 54 Suppl:S213 (2004)]
