Tumour necrosis factor-α potentiates contraction of human bronchusin vitro

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Abstract
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-α (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. 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. 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. 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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