Tumour necrosis factor-α potentiates contraction of human bronchus in vitro

Publication Type:
Journal Article
Citation:
Respirology, 2001, 6 (3), pp. 199 - 203
Issue Date:
2001-10-06
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Objective: Chronic inflammation of the airways is an important component in the induction of airway hyperresponsiveness (AHR) in asthma. The pro-inflammatory cytokines interleukin-1β (IL-1β) and tumour necrosis factor-cc (TNF-α) have been implicated in the induction of AHR. Whether these cytokines directly modulate the contractile properties of human airway smooth muscle (ASM) has not been fully investigated. Methodology: The contractile response to acetylcholine (ACh) (10-8 to 10-3 mol/L) was determined in isolated human bronchial segments both prior to and following a 16-h incubation period with IL-1β (10 or 20 ng/mL) and TNF-α (25 ng/mL), either alone or in combination. Incubation of human bronchial segments with IL-1β/TNF-α was also performed in the presence of the COX-1/COX-2 inhibitor, indomethacin. Results: Tumour necrosis factor-α potentiated the contractile response to ACh by approximately 27%, while IL-1β or the cytokines in combination had no effect. Indomethacin had no modulatory effect on the contractile response to ACh in the cytokine-treated tissues. Conclusions: The relative concentrations of IL-1β/TNF-α in the vicinity of ASM may ultimately determine their effects on ASM contraction in asthma.
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