Article Figures & Data
Figures
- Fig. 1.
The effect of LPS on rectal temperature and CGRP content in tissues. A, The time course of rat rectal temperature before and after intraperitoneal injection of saline or LPS (0.75 mg/kg). The data are presented as mean ± SEM of five to six animals in each group. **p < 0.01, ***p < 0.001, unpaired t test; LPS group versus saline group in the same time point. B, The concentration of CGRP (fmol/mg tissue) in the rat trachea;C, the CGRP concentration (fmol/mg protein) in vagus nerve 2 and 5 hr after intraperitoneal injection of LPS (0.75 mg/kg) or 5 hr after intraperitoneal injection of saline. *p < 0.05, one-way ANOVA; LPS 5 hr versus saline group.
- Fig. 2.
The effect of LPS on tracheal CGRP release. CGRP concentration (fmol/10 min fraction) in the perfusates from intraluminally perfused rat trachea by capsaicin (Caps, 0.1 μm) in control group (A), in LPS-treated rats (0.75 mg/kg, i.p.) 2 hr after drug administration (B), and LPS-treated animals (0.75 mg/kg, i.p.) 5 hr after drug administration (C), and LPS (10 μg/ml) was applied directly to the tracheas in untreated rats (D).Basal, Perfused with Krebs’ buffer; n = 8–10/group. *p < 0.05, one-way ANOVA; LPS 5 hr versus saline group.
- Fig. 3.
Antagonism of the potentiating effect of LPS. Effects of IL-1β antagonist: Lys-d-Pro-Thr or cyclooxygenase inhibitors ketorolac (Keto) or indomethacin (Indo) on capsaicin-evoked (0.1 μm) CGRP release (Δfmol/10 min fraction, basal levels were subtracted) in the tracheas of LPS-treated or saline-treated (No LPS) animals. No Ant, No antagonist; n = 4–10/group; *p < 0.05, **p < 0.01, one-way ANOVA.
- Fig. 4.
Basal and capsaicin-evoked release of CGRP by IL-1β. Basal CGRP release (A) (fmol/10 min fraction) and capsaicin-evoked (0.1 μm) CGRP release (B) (Δfmol/10 min fraction) from intraluminally perfused rat trachea in presence of IL-1β (1–10,000 pg/ml). Control, Absence of IL-1β; n = 4–12/each group; **p < 0.01, one-way ANOVA, IL-1β versus control.
- Fig. 5.
Basal and capsaicin-evoked release of CGRP by TNF-α. Basal CGRP release (A) (fmol/10 min fraction) and capsaicin-evoked (0.1 μm) CGRP release (B) (Δfmol/10 min fraction) from intraluminally perfused rat trachea in presence of TNF-α (10–10,000 pg/ml). Control, Absence of TNF-α; n = 4–16/each group; *p < 0.05, one-way ANOVA, TNF-α versus control.
- Fig. 6.
Antagonism of the potentiating effect of IL-1β. Effects of IL-1β antagonist Lys-d-Pro-Thr (50 μm) or cyclooxygenase inhibitor ketorolac (Keto, 10 μm) on IL-1β-potentiated (10 pg/ml) CGRP release by capsaicin (0.1 μm) (Δfmol/10 min fraction, basal level were subtracted);n = 6–16/group; *p < 0.05, one-way ANOVA.
