Plasma exudation in the airways: mechanisms and function

Inflammatory challenges of tracheobronchial and nasal mucosa produce prompt extravasation or exudation of plasma from the well developed microcirculation just beneath the epithelial base. Plasma exudation is not an exaggeration of the normal capilliary exchange of fluid and solutes but a specific inflammatory response of post-capilliary venules. The exuded plasma may not produce oedema. By a rapid, undirectional, unfiltered and yet non-injurious process, plasma exudates cross the mucosal lining to appear on the airway surface at the site of challenge. In vitro data suggests the possibility that a slightly increased hydrostatic pressure moves the acellular exudate through valve-like openings between epithelial cells. By the venular-mucosal exudation mechanism all the potent protein systems of circulating plasma will operate in respiratory defence on the surface of an intact mucosa. A further inference is that exudative indices obtained from the airway surface quantitatively reflect the intensity and time course of mucosal/submucosal inflammatory processes. Irrespective of which particular cellular mechanism happens to fuel the inflammation. Mucosal exudation of plasma characteristically occurs in health and disease also when there is no airway oedema, no epithelial disruption, and no increased absorbtion ability. However, exuded plasma and its derived peptide mediators potentially contribute to several pathophysical and pathophysiological characteristics of inflammatory airway diseases.

This article has been cited by other articles:

				M. E. Friscia, J. Zhu, J. W. Kolff, Z. Chen, L. R. Kaiser, C. S. Deutschman, and J. B. Shrager Cytokine Response is Lower After Lung Volume Reduction Through Bilateral Thoracoscopy Versus Sternotomy Ann. Thorac. Surg., January 1, 2007; 83(1): 252 - 256. [Abstract] [Full Text] [PDF]

				K. D. Elder and E. T. Harvill Strain-Dependent Role of BrkA during Bordetella pertussis Infection of the Murine Respiratory Tract Infect. Immun., October 1, 2004; 72(10): 5919 - 5924. [Abstract] [Full Text] [PDF]

				M. G. Barnes and A. A. Weiss BrkA Protein of Bordetella pertussis Inhibits the Classical Pathway of Complement after C1 Deposition Infect. Immun., May 1, 2001; 69(5): 3067 - 3072. [Abstract] [Full Text] [PDF]

				C. HERMANS and A. BERNARD Lung Epithelium-specific Proteins . Characteristics and Potential Applications as Markers Am. J. Respir. Crit. Care Med., February 1, 1999; 159(2): 646 - 678. [Full Text]