Mucus transport and inflammation.
Mechanisms which disturb mucociliary transport may act on the mucus, the ciliary action or both. Inflammation of the airways almost invariably induces reversible functional disturbances but can, in chronic diseases, also lead to irreversible morphological lesions. Infectious inflammation acts mainly through ciliostatic or cytotoxic effects on ciliated cells. Infections with rhinovirus, influenza virus A and M. pneumoniae may induce profound disturbances of the mucociliary system, with effects lasting up to 1 year. In non-infectious inflammation, the mucociliary system might be influenced by serum factors leaking through the bronchial wall, by inflammatory cells such as granulocytes and eosinophils, and by mediators released from mast cells. In a very early phase of the acute allergic reaction in bronchial asthma, these mediators are responsible for an acceleration of mucus transport, which is followed by a long-standing depression mainly due to the production of highly viscous mucus. Any positive therapeutic effects resulting from drug administration can only be achieved in early phases of the disease, before irreversible morphological lesions have occurred.
D001693:Biological Transport, Active; D002923:Cilia / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*; D008854:Microscopy, Electron; D008855:Microscopy, Electron, Scanning; D009092:Mucous Membrane / Q000473:pathology; D009093:Mucus / Q000502:physiology*; D011877:Radionuclide Imaging; D012143:Respiratory Physiological Phenomena; D012141:Respiratory Tract Infections / Q000503:physiopathology