Pulmonary Host Defenses

Protective mechanisms spaced along the entire respiratory tract largely prevent noxious substances and particles inspired or aspirated into the lungs from injuring the mucosa and the delicate alveolar surface. Airway disease, especially infection, is infrequent and usually not serious for most humans, considering the virtually constant exposure to microbes. When it does occur, some malfunction or deficiency in host defense mechanisms may be the culprit. This requires medical investigation to identify the defect and possibly to correct it. The causal relationship between microbe and pulmonary disease (bronchitis and pneumonia) has stimulated considerable research directed to the infectious agents and to mechanisms the respiratory tract uses to defend itself. This concept was nicely integrated by Green in 1970, 1 Green GM The J Burns Amberson Lecture—In defense of lung. Am Rev Respir Dis. 1970; 703: 102-691 Google Scholar based largely on results from experimental animal models, and became a framework for subsequent research with human materials. Although beginning in the late ’60s with washing the airways through the rigid bronchoscope or balloon anchored catheters (Metras), the decade of the 70s witnessed the flourishing of lung lavage with the advent of flexible fiberoptic bronchoscopy. This permitted multiple samples from the alveolar surface which provided an indirect view at least of the air-exchange surface through the retrieval of proteins, lipoproteins, and detachable cells. 2 Reynolds HY Bronchoalveolar lavage—state of the art. Am Rev Respir Dis. 1987; 63: 135-250 Google Scholar Such was the “state of the art” in 1978 at the 21st Aspen Lung Conference on “Immunology of the Lung,” when I had the opportunity to review this topic, lung host defenses. 3 Reynolds HY Lung host defenses: a status report. Chest. 1979; 42S: 75-239 Google Scholar That report constructed a bridge between animal data, especially on immune responses in the lungs, and human results that had accumulated after approximately 6 y of BAL experience in normal human volunteers and in some patients with lung infections. A complete inventory of proteinaceous and cellular components on the alveolar surface was given, ingredients for macrophage phagocytosis (including opsonins and macrophage membrane receptors) were discussed, and the kinetics of the inflammation via chemotaxins were presented. An attempt was made to emphasize that abnormalities in one of several host mechanisms could be the cause of infection or lung injury and that identifying the defect and devising replacement therapy or augmenting a compensatory host mechanism would be the strategy of future treatment.