Figure 2

Measurement of interleukin-6 (IL-6; A) and tumour necrosis factor-α (TNF-α; B) in groups of mice: untreated ( NT ); unilateral nasal wash with Triton X-100 alone ( TX ); unilateral nasal wash with Triton X-100 followed by saline wash ( TXS ); unilateral nasal wash with Triton X-100 followed by S. aureus inoculation ( TXB ). Undamaged normal olfactory tissues express negligible amounts of IL-6 and TNF-α. At 4 days post-Triton X-100 damage (TX), olfactory tissues had an initial expression of IL-6 and TNF-α of 3,309 ± 1,052 pg/ml and 49 ± 6 pg/ml respectively. The level of IL-6 is significantly increased by the presence of bacteria at the 24-h time point (12,466 ± 956 pg/ml). The upregulation of IL-6 appears to follow that of TNF-α, which occurs at the 6-h time point, albeit at a lower concentration (1,024 ± 137 pg/ml). Thereafter, at the 24-h time point, a decreasing trend in TNF-α production is observed. Error bars represent SEM. *p < 0.05; **p < 0.01. IL-6 expression in the olfactory mucosa (C) and olfactory bulb (D) 24 h post-inoculation with S. aureus. IL-6 immunoreactivity is present in the cytoplasm of select groups of supporting cells in the apical part of the olfactory epithelium (OE). Some cells straddling the OE and lamina propria (LP), possibly OECs or macrophages, express IL-6 (large arrow), while others do not (small arrow). Several cells in the LP are immunopositive for IL-6 including some that surround the small lumen (arrowheads), which are most likely endothelial cells or inflammatory cells. Inset shows immunoreactivity for IL-6 in cultured OECs. White arrowhead at the edge of the micrograph indicates location of basal lamina. In the olfactory bulb mitral cell soma (arrows) show positive immunostaining for IL-6 with more diffuse staining in the external plexiform layer (EPL). GrL = granule cell layer; scale bar = 40 μm (inset in C); 50 μm (C,D).