Ketoprofen Lysinate exerts anti-inflammatory activity and preserves barrier function in injured primary bronchial epithelial cells

The airway epithelium provides a barrier to the external environment and activates multiple cellular signaling in response to pathogens or environmental agents. Viral infections of the respiratory tract are frequently the cause of exacerbations in asthma and COPD. Following viral infections, airway epithelial cells activate an innate immune response with release of inflammatory cytokines such as IL-8 and this event is associated to alterations in the structural proteins of the tight junctions and loss of the barrier function of the epithelium. Ketoprofen Lysinate (Keto) is one of the most commonly used non-steroidal anti-inflammatory drugs (NSAIDs) useful to manage symptoms of viral respiratory infections. The molecular mechanisms through which Keto acts at the level of the respiratory epithelium are little known. The aim of this study was to evaluate, for the first time, the effect of Keto on inflammation and on the expression of tight junctions molecules, using a model of primary bronchial epithelial cells exposed to a mix of cytokines and PolyIC or to cigarette smoke and PolyIC to reproduces exacerbation milieu of asthma or COPD. It was evaluated: cell viability, IL-8 release and expression of molecules of tigh junction. At the biocompatible dose, Keto increases intercellular junction molecules improving epithelium barrier function and mitigated the release of IL-8 induced by cigarette smoke, cigarette smoke and PolyIC, exerting an anti-inflammatory effect. In conclusion, the Keto exerts an anti-inflammatory and stabilizing effect on the epithelium thus representing a valid tool to support the management of respiratory infections.