Background. Airway smooth muscle cells (ASMC) play a major role in airway inflammation, hyperresponsiveness and obstruction in asthma. However, very little is known regarding the relation between inflammatory mediators or cytokines and immature ASMC. Aim. To evaluate the 1) secretion of LIF (an IL-6 family neurotrophic cytokine) by ASMC; 2) intracellular calcium [Ca²⁺]i signalling, and 3) the effect of LIF on mast-cell chemotaxis and rat airway contractility. Material & Methods. Immature and adult human ASMC were cultured. ELISA and real-time PCR were performed to assess LIF protein secretion and mRNA production, [methyl-3 H]thymidine incorporation to quantify ASMC DNA synthesis, a Boyden chamber to evaluate the effect of LIF on mast-cell chemotaxis, microspectroflurimetry using indo-1 (at baseline and after stimulation by bradykinin, U46619, histamine and acetylcholine, in the presence or absence of LIF or TNF) for [Ca²⁺]i signalling, and isolated rat pup tracheae to determine the effect of LIF on airway contractility to ACh. Results. TNF-stimulated immature ASMC produce more LIF mRNA and protein than adult ASMC, although this cytokine induces a moderate increase in DNA synthesis (+20 %) in adult ASMC only. Human recombinant hrLIF exerts no chemotactic effect on human mast cells. In immature ASMC, ACh-induced [Ca²⁺]i response was enhanced twofold after incubation with LIF, while TNF increased threefold the [Ca²⁺]i to U46619. In TNF-exposed adult ASMC, [Ca²⁺]i responses to acetylcholine were of greater magnitude (sixfold increase) than in immature ASMC. hrLIF increased contractility to ACh by 50 % in immature isolated rat tracheae. Conclusion. Stimulated immature human ASMC greatly secrete LIF, thus potentially contributing to neuro-immune airway inflammation and subsequent remodeling. Increased LIF secretion enhances airway reactivity and intracellular calcium signalling.