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Volume 16, Number 15,
Issue of August 1, 1996
pp. 4742-4748
Copyright ©1996 Society for Neuroscience
Involvement of Cytokines in Lipopolysaccharide-Induced
Facilitation of CGRP Release from Capsaicin-Sensitive Nerves in the
Trachea: Studies with Interleukin-1 and Tumor Necrosis
Factor-
Received March 22, 1996; revised April 30, 1996; accepted May 3, 1996.
Xiao-Ying Hua1,
Ping Chen1,
Alyson Fox2, and
Robert R. Myers1
1 Department of Anesthesiology, University of
California, San Diego, La Jolla, California 92093-0818, and
2 National Heart and Lung Institute, London SW3 6LY, United
Kingdom
Lipopolysaccharide (LPS), an endotoxin, produces pain behavior,
inflammation, and changes in immune function. Many of these effects are
secondary to the production of cytokines. In the present study, we
investigated the effect of LPS on the releasing function of afferent
terminals as measured by calcitonin gene-related peptide (CGRP) release
in ex vivo perfused rat trachea, and examined the possible
role of the cytokines interleukin-1 (IL-1) and tumor necrosis
factor- (TNF-) as intermediaries in this effect. Systemic
injection of LPS (0.75 mg/kg, i.p.) in adult rats induced an increase
in body temperature followed by hypothermia, indicating ongoing
infection. We observed that capsaicin-induced (0.1 µM) tracheal CGRP release was significantly
enhanced in the LPS-treated animals after 5 hr. This enhancement of the
peptide release by LPS was blocked by IL-1 tripeptide antagonist
Lys-D-Pro-Thr (10 µM) and
mimicked by IL-1 and TNF- (10-100 pg/ml), suggesting that the
potentiating effect of LPS on CGRP release is mediated by generation of
IL-1 and TNF-. IL-1-induced augmentation of CGRP release was
blocked by Lys-D-Pro-Thr. Additionally, the
cyclooxygenase inhibitor ketorolac (10 µM)
significantly attenuated the facilitatory effects of LPS and IL-1,
indicating involvement of prostanoids. These findings suggest that
endotoxin treatment generated cytokines such as IL-1 and TNF-
that regulated the peripheral releasing function of primary sensory
afferents by sensitizing the terminals and facilitating peptide
release. This effect is prostanoid dependent.
Key words:
sensory nerves;
calcitonin gene-related peptide;
lipopolysaccharide;
interleukin-1;
tumor necrosis factor-;
trachea
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