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      Alveolar epithelial type II cell: defender of the alveolus revisited

      review-article
      Author(s): 1 ,
      Publication date (Electronic):
      Journal: Respiratory Research
      Publisher: BioMed Central
      Keywords: alveolar epithelium, apoptosis, cell–cell interactions, repair, surfactant

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          Abstract

          In 1977, Mason and Williams developed the concept of the alveolar epithelial type II (AE2) cell as a defender of the alveolus. It is well known that AE2 cells synthesise, secrete, and recycle all components of the surfactant that regulates alveolar surface tension in mammalian lungs. AE2 cells influence extracellular surfactant transformation by regulating, for example, pH and [Ca 2+] of the hypophase. AE2 cells play various roles in alveolar fluid balance, coagulation/fibrinolysis, and host defence. AE2 cells proliferate, differentiate into AE1 cells, and remove apoptotic AE2 cells by phagocytosis, thus contributing to epithelial repair. AE2 cells may act as immunoregulatory cells. AE2 cells interact with resident and mobile cells, either directly by membrane contact or indirectly via cytokines/growth factors and their receptors, thus representing an integrative unit within the alveolus. Although most data support the concept, the controversy about the character of hyperplastic AE2 cells, reported to synthesise profibrotic factors, proscribes drawing a definite conclusion today.

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          Most cited references272

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          Pulmonary surfactant in health and human lung diseases: state of the art.

          M Griese (1999)
          Pulmonary surfactant is a complex and highly surface active material composed of lipids and proteins which is found in the fluid lining the alveolar surface of the lungs. Surfactant prevents alveolar collapse at low lung volume, and preserves bronchiolar patency during normal and forced respiration (biophysical functions). In addition, it is involved in the protection of the lungs from injuries and infections caused by inhaled particles and micro-organisms (immunological, non-biophysical functions). Pulmonary surfactant can only be harvested by lavage procedures, which may disrupt its pre-existing biophysical and biochemical micro-organization. These limitations must always be considered when interpreting ex vivo studies of pulmonary surfactant. A pathophysiological role for surfactant was first appreciated in premature infants with respiratory distress syndrome and hyaline membrane disease, a condition which is nowadays routinely treated with exogenous surfactant replacement. Biochemical surfactant abnormalities of varying degrees have been described in obstructive lung diseases (asthma, bronchiolitis, chronic obstructive pulmonary disease, and following lung transplantation), infectious and suppurative lung diseases (cystic fibrosis, pneumonia, and human immunodeficiency virus), adult respiratory distress syndrome, pulmonary oedema, other diseases specific to infants (chronic lung disease of prematurity, and surfactant protein-B deficiency), interstitial lung diseases (sarcoidosis, idiopathic pulmonary fibrosis, and hypersensitivity pneumonitis), pulmonary alveolar proteinosis, following cardiopulmonary bypass, and in smokers. For some pulmonary conditions surfactant replacement therapy is on the horizon, but for the majority much more needs to be learnt about the pathophysiological role the observed surfactant abnormalities may have.
          Article 0 comments Cited 116 times – based on 0 reviews     Review now
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            Cell number and cell characteristics of the normal human lung.

            James Crapo, P Gehr, B Barry … (1982)
            Eight normal human lungs obtained from patients dying from causes not related to the lung were subjected to morphometric analysis to determine the number of cells in the alveolar region and their mean volume and surface characteristics. The age range was 19 to 40 yr, average body weight was 74 kg, and the average fixed lung volume was 4,300 ml. The overall mean nuclear diameters of the nuclei of 5 major cell types in the lung parenchyma were found to have little variation, with means ranging from 7.54 to 8.77 micrometers. Alveolar type I epithelial cells were found to comprise 8% of the cells and to be one of the largest cells, having a mean volume of 1,764 micrometers 3 and covering an average of 5,098 micrometers 2 of alveolar surface. Seven percent of the alveolar surface was covered by alveolar type II cells, which make up 16% of the total alveolar cells and have a mean volume that is half that of the type I pneumocyte. Capillary endothelial cells make up 30% of the lung cells and were significantly smaller in both size and average surface area than the alveolar type I cells. Cells in the interstitial space comprised 37% of the total cells. The number of alveolar macrophages showed great variability, ranging from 19% of alveolar cells in 1 person to 3 to 5% in the nonsmoking females. The alveolar cell population characteristics found in resected lobes from 2 nonsmoking females were found to be similar to 2 nonsmoking females studied after autopsy. An interspecies comparison of characteristics of cells from the alveolar regions of normal lungs from humans, baboons, and rats showed that proportions of cells in the alveolar region and their average thickness, size, and surface areas were relatively constant.
            Article 0 comments Cited 106 times – based on 0 reviews     Review now
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              Granulocyte apoptosis and its role in the resolution and control of lung inflammation.

              C Haslett (1999)
              Elucidation of the poorly understood mechanisms by which acute inflammation normally resolves is likely to provide new insights into the pathogenesis of persistent inflammatory states that characterize inflammatory disease and generate new therapeutic targets. We have concentrated on the mechanisms by which granulocytes and their histotoxic contents are cleared from inflamed sites during resolution. Although it had been assumed that extravasated neutrophils disintegrated (undergo necrosis) in situ, we have demonstrated an alternative fate, whereby the cell undergoes apoptosis, a process that has different implications for the control of inflammation. During apoptosis the neutrophil retains its granule contents and loses the ability to secrete them in response to secretagogues. In contrast to necrotic neutrophils, apoptotic neutrophils are ingested by inflammatory macrophages employing novel phagocytic recognition mechanisms that fail to provoke a macrophage proinflammatory response. These recognition mechanisms can be modulated by a number of environmental factors and may represent a pivotal point in the control of inflammation, since if apoptotic granulocytes are not rapidly cleared they undergo secondary necrosis with all the detrimental consequences entailed. The apoptotic clearance pathway is also available to eosinophil granulocytes, but our work suggests that the internal controls may be different from those in neutrophils. For example, corticosteroids delay neutrophil apoptosis but greatly accelerate eosinophil apoptosis, in what may represent a previously unsuspected beneficial mechanism of steroid action in allergic diseases such as bronchial asthma. Furthermore, such differences may lead to novel therapies based on the specific induction of eosinophil apoptosis. Haslett C. Granulocyte apoptosis and its role in the resolution and control of lung inflammation.
              Article 0 comments Cited 78 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Respir Res
                Title: Respiratory Research
                Publisher: BioMed Central
                ISSN (Print): 1465-9921
                ISSN (Electronic): 1465-993X
                Publication date (Print): 2001
                Publication date (Electronic): 15 January 2001
                Volume: 2
                Issue: 1
                Pages: 33-46
                Affiliations
                [1 ]Institute of Pathology, University Clinics "Carl Gustav Carus", Technical University of Dresden, Germany
                Article
                Publisher ID: rr36
                DOI: 10.1186/rr36
                PMC ID: 59567
                PubMed ID: 11686863
                SO-VID: 711d0846-fa87-4cd6-b261-41abc655f2e6
                Copyright © Copyright © 2001 BioMed Central Ltd
                History
                Date received : 27 October 2000
                Date revision requested : 21 November 2000
                Date revision received : 5 December 2000
                Date accepted : 6 December 2000
                Categories
                Subject: Review

                ScienceOpen disciplines: Respiratory medicine
                Keywords: surfactant,cell–cell interactions,alveolar epithelium,apoptosis,repair
                Data availability:
                ScienceOpen disciplines: Respiratory medicine
                Keywords: surfactant, cell–cell interactions, alveolar epithelium, apoptosis, repair

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