title: Acquired cilia dysfunction in chronic rhinosinusitis.
abstract: BACKGROUND
  Cilia are complex and powerful cellular structures of the respiratory mucosa that play a critical role in airway defense. Respiratory epithelium is lined with cilia that perform an integrated and coordinated mechanism called mucociliary clearance. Mucociliary  clearance is the process by which cilia transport the mucus blanket overlying respiratory mucosa to the gastrointestinal tract for ingestion. It is the primary means by which the airway clears pathogens, allergens, debris, and toxins. The complex structure and regulatory mechanisms that dictate  the form and function of normal cilia are not entirely understood, but it is clear that ciliary dysfunction results in impaired respiratory defense.
  
  
  METHODS
  A literature review of the current knowledge of cilia dysfunction in chronic rhinosinsusitis was conducted.
  
  
  RESULTS
  Ciliary dysfunction may be primary, the result of genetic mutations resulting in abnormal cilia structure, or, more commonly, secondary, the result of environmental, infectious, or inflammatory stimuli that disrupt normal motility or coordination. Patients with chronic  rhinosinusitis (CRS) have been found to have impaired mucociliary clearance. Many biochemical, environmental, and mechanical stimuli have been shown to influence ciliary beat frequency, and common microbial pathogens of respiratory mucosa such as Pseudomonas aeruginosa and Haemophilus influenzae  have developed toxins that appear to interrupt normal mucociliary function. Furthermore, inflammatory mediators known to be present in patients with CRS appear to impair secondarily mucociliary clearance.
  
  
  CONCLUSIONS
  The goal of this article is to summarize the recent developments  in the understanding of cilia dysfunction and mucociliary clearance in CRS.
authors.affiliation: Department of Otorhinolaryngology-Head and Neck Surgery, University of Pennsylvania, 3400 Spruce Street, Philadelphia, PA 19104, USA.
authors.forename: David
authors.initials: D
authors.lastname: Gudis
authors.forename: Ke-qing
authors.initials: KQ
authors.lastname: Zhao
authors.forename: Noam A
authors.initials: NA
authors.lastname: Cohen
mesh_terms: D000818:Animals; D002908:Chronic Disease; D002923:Cilia / Q000473:pathology / Q000502:physiology; D006801:Humans; D018928:Immunity, Mucosal; D018836:Inflammation Mediators / Q000378:metabolism; D009079:Mucociliary Clearance; D020545:Respiratory Mucosa / Q000473:pathology / Q000503:physiopathology; D012141:Respiratory Tract Infections / Q000473:pathology / Q000503:physiopathology*; D012220:Rhinitis / Q000473:pathology / Q000503:physiopathology*; D015398:Signal Transduction; D012852:Sinusitis / Q000473:pathology / Q000503:physiopathology*
chemical_list: D018836:Inflammation Mediators