Lung defence mechanisms against infection.

The respiratory tract must be open to the environment to allow exchange of gas between air and blood. This renders lhe lungs susceptible to colonization and infection by foreign organisms. It is necessary for lhe lower respiratory tract to have mechanisms to contain and control such foreign material. The gas exchange surface of lhe lung must be thin, delicate and permeable, rhus the mechanisms involved in clearing secretions must cause relatively little inflammation or damage. These mechanisms are briefly reviewed. Inspired gas meets resistance to flow in the nose and mouth which causes a turbulent flow pattem. This turbulence deflects particles contained in the gas or secretions against the mucosal surfaces of the upper airway. The lung is proteCted by its anatomical pattem of branching coupled with the turbulent flow in large airways, which causes further interaction of particles with the mucosal surface, specifically near airway branch points. These phenomena successfully remove most particles larger than 10 J.L in size. The airway mucosal surfaces are lined by pseudostratified, columnar epithelium which has two important characteristics: 1) numerous glandular cells, which can be stimulated by physical mechanisms to release mucus, which traps inhaled particles; 2) cilia, which beat at approximately 5 Hz in a co-ordinated fashion to propel foreign material and mucus towards the mouth. Secretions can be expelled from the respiratory tract by vigorous coughing. The respiratory pressures of cough (which exceed 100 mmHg) can cause flow rates great enough to dislodge most large particles of mucus from the airways into the upper respiratory tract [1, 2]. The secretions in the lower respiratory tract are complex and include substances which pass by transudation from the serum across the basement membrane. Other soluble components on the air side of the lung have been synthesized by cells in the lower respiratory tract or secreted into the lung by relatively complex mechanisms e.g. IgG and the complement proteins may move passively from serum into respiratory tract secretions by diffusion. However, in some situations these proteins may be locally synthesized within the lung. By contrast, IgA is synthesized by plasma cells in sub-mucosal areas of the larger airways and undergoes a specific transport process across the mucosal surface to the luminal side of the membrane (3]. Several substances are important in pulmonary defence against infection. Active or passive immunization against Gram-negative organisms may dramatically alter the outcome of Gram-negative pneumonia [4, 5). The host defence against viral infection can be related to the presence of specific lgA antibody in the respiratory secretions. Complement proteins arc important in t11e host defence system. They can be activated by immune complexes via the direct pathway in previously