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Role of Epithelial ICAM-1 in Endotoxin-Induced Lung Injury

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Intensive Care Medicine

Abstract

Distal airway epithelial cells, alveolar epithelial cells, are vital for maintenance of the pulmonary air-blood barrier. Gaseous diffusion occurs across alveolar type I cells, large thin cells that cover the majority of the alveolar surface. Type II cells are cuboidal cells, which produce pulmonary surfactant. They are also progenitor cells capable of proliferating and differentiating into type I cells [1]. Recent evidence suggests that airway epithelial cells might also act as immune effector cells in response to noxious endogenous or exogenous stimuli. Several studies have shown that airway epithelial cells express and secrete various immune molecules such as adhesion molecules, cytokines and chemokines. Through the expression and production of these inflammatory mediators, the airway epithelium is thought to play an important role in the initiation and exacerbation of inflammatory response within the airway.

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Authors
  1. B. Beck-Schimmer
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  2. R. C. Schimmer
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  3. T. Pasch
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Editor information

Editors and Affiliations

  1. Department of Intensive Care, Erasme Hospital, Free University of Brussels, Route de Lennik 808, B-1070, Brussels, Belgium

    Jean-Louis Vincent MD, PhD, FCCM, FCCP (Head) (Head)

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© 2003 Springer-Verlag Berlin Heidelberg

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Beck-Schimmer, B., Schimmer, R.C., Pasch, T. (2003). Role of Epithelial ICAM-1 in Endotoxin-Induced Lung Injury. In: Vincent, JL. (eds) Intensive Care Medicine. Springer, New York, NY. https://doi.org/10.1007/978-1-4757-5548-0_1

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  • DOI: https://doi.org/10.1007/978-1-4757-5548-0_1

  • Publisher Name: Springer, New York, NY

  • Print ISBN: 978-1-4757-5550-3

  • Online ISBN: 978-1-4757-5548-0

  • eBook Packages: Springer Book Archive

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