Tumor Necrosis Factor-Alpha (TNF-α) Stimulates Mucin Secretion and Gene Expression in Airway Epithelium In Vitro (original) (raw)

The animals subsequently were anesthetized with pentobarbital, tracheostomized, and respiratory system resistance was determined via body plethysmography. Airway responsiveness was assessed by determining the concentration of nebulized methacholine that produced a 100% increase in respiratory system resistance (PClOO). No difference was noticed in baseline resistance between test or control animals. However, animals receiving rhiL-11 demonstrated a significant lower log PClOO, thus more reactivity to methacholine, at 24 h (0.51 ± 0.15 vs 2.45 ± 0.32 mg/ mL, p<0.005) and 48 h (0.49±0.20 vs 3.0±0.1 mg/ mL, p<0.005) after administration. These studies demonstrate that RSV, parainfluenza virus type 3, and rhinovirus are not only potent but are also, in part, specific inducers of IL-11 production in lung stromal cells. Furthermore, IL-11 can be detected in nasal secretions of children presenting with viral-like upper respiratory tract symptoms. Finally IL-11 can induce airway hyperresponsiveness when administered locally to the airways of BALB/c mice. We, therefore, conclude that IL-11 may be an important mediator of airway hyperresponsiveness associated with viral infections of the respiratory tract. REFERENCES

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