Club cell

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Club cell
Latin exocrinocytus bronchiolaris
Code TH H3.

Club cells are dome-shaped cells with short microvilli found in the small airways (bronchioles) of the lungs.[1] Club cells were called Clara cells until it was decided to rename them with effect from January 2013. Club cells are found in the ciliated simple epithelium. These cells may secrete glycosaminoglycans to protect the bronchiole lining. Bronchiolar cells gradually increase in number as the number of goblet cells decrease.

They are also known by their descriptive name of "bronchiolar exocrine cells".[2]


Club cells were previously called Clara cells as they were originally described by their namesake, Max Clara in 1937. Clara was born in South Tyrol in 1899 and died in 1966. He was a Nazi doctor who used tissue from executed victims of the Third Reich for his research at Leipzig, including the work that led to his discovery of Clara cells.[3] It was for this reason that in May 2012, the Respiratory Journal Editors (comprising the editors of most of the major respiratory journals, including the journals of the American Thoracic Society, the European Respiratory Society and the American College of Chest Physicians) agreed to adopt a name change policy starting on January 1, 2013.[4] It had previously been agreed that the term "Clara" be used parenthetically for a 2-year period before the final adoption of club cell. Clara cell and Clara cell secretory protein were to be replaced with club cell and club cell secretory protein, respectively.[5]

One of the main functions of club cells is to protect the bronchiolar epithelium. They do this by secreting a small variety of products, including club cell secretory protein uteroglobin, and a solution similar to the component of the lung surfactant. They are also responsible for detoxifying harmful substances inhaled into the lungs. Club cells accomplish this with cytochrome P450 enzymes found in their smooth endoplasmic reticulum. Club cells also act as a stem cell and multiply and differentiate into ciliated cells to regenerate the bronchiolar epithelium.[6]


The respiratory bronchioles represent the transition from the conducting portion to the respiratory portion of the respiratory system. The narrow channels are usually less than 2 mm in diameter and they are lined by a simple cuboidal epithelium, consisting of ciliated cells and non-ciliated club cells, which are unique to bronchioles. In addition to being structurally diverse, club cells are also functionally variable. One major function they carry out is the synthesis and secretion of the material lining the bronchiolar lumen. This material includes glycosaminoglycans, proteins such as lysozymes, and conjugation of the secretory portion of IgA antibodies. These play an important defensive role, and they also contribute to the degradation of the mucus produced by the upper airways. The heterogeneous nature of the dense granules within the club cell's cytoplasm suggests that they may not all have a secretory function. Some of them may contain lysosomal enzymes, which carry out a digestive role, either in defense: Club cells engulf airborne toxins and break them down via their cytochrome P-450 enzymes (particularly CYP4B1, which is only present in the club cells) present in their smooth endoplasmic reticulum; or in the recycling of secretory products. Club cells are mitotically active cells. They divide and differentiate to form both ciliated and non-ciliated epithelial cells.

Role in disease[edit]

Club cells contain tryptase, which is believed to be responsible for cleaving the hemagglutinin surface protein of influenza A virus, thereby activating it and causing the symptoms of flu.[7] When the l7Rn6 protein is disrupted in mice, these mice display severe emphysema at birth as a result of disorganization of the Golgi apparatus and formation of aberrant vesicular structures within clara cells.[8] Malignant club cells are also seen in bronchioalveolar carcinoma of the lung

See also[edit]


  1. ^ Atkinson JJ, Adair-Kirk TL, Kelley DG, Demello D, Senior RM (2008). "Clara cell adhesion and migration to extracellular matrix". Respir. Res. 9 (1): 1. doi:10.1186/1465-9921-9-1. PMC 2249579. PMID 18179694. 
  2. ^ Peter J. Papadakos; Burkhard Lachmann (29 August 2007). Mechanical Ventilation: Clinical Applications and Pathophysiology. Elsevier Health Sciences. pp. 74–. ISBN 978-0-7216-0186-1. Retrieved 27 May 2011. 
  3. ^ Winkelmann, Andreas; Noack, Thorsten (2010). "The Clara cell - a "Third Reich eponym"?". European Respiratory Journal 36 (4): 722–7. doi:10.1183/09031936.00146609. PMID 20223917. 
  4. ^ Irwin, RS; Augustyn N, French CT, Rice J, Tedeschi V, Welch SJ (2013). "Spread the word about the journal in 2013: from citation manipulation to invalidation of patient-reported outcomes measures to renaming the Clara cell to new journal features". Chest 143: 1–5. PMID 23276834. 
  5. ^ Akram, KM; Lomas NJ, Spiteri MA, Forsyth NR (2013). "Club cells inhibit alveolar epithelial wound repair via TRAIL-dependent apoptosis". Eur Respir J 41: 683–694. doi:10.1183/09031936.00213411. PMID 22790912. 
  6. ^
  7. ^ Taubenberger JK (August 1998). "Influenza virus hemagglutinin cleavage into HA1, HA2: No laughing matter". Proc. Natl. Acad. Sci. U.S.A. 95 (17): 9713–5. doi:10.1073/pnas.95.17.9713. PMC 33880. PMID 9707539. 
  8. ^ Fernández-Valdivia R, Zhang Y, Pai S, Metzker ML, Schumacher A (January 2006). "l7Rn6 Encodes a Novel Protein Required for Clara Cell Function in Mouse Lung Development". Genetics 172 (1): 389–99. doi:10.1534/genetics.105.048736. PMC 1456166. PMID 16157679. 

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