Respiratory tract defense mechanisms

Widdicombe, J, G. (1977). Defense mechanisms of the respiratory tract and lungs. In International Review of Physiology Volume 14. Repiratory Physiology U (J. G. Widdicombe, Ed.), pp. 291-316. University Park Press, Baltimore. [Pg.231]

Respiratory infections caused by P. aeruginosa occur almost exclusively in individuals with a compromised lower respiratory tract or a compromised systemic defense mechanism. The infection of CF patients by mucoid strains of P. aeruginosa is common and is difficult - if not impossible - to treat. Therefore, mondoBIOTECH is currently developing therapeutic bacteriophages specific for the eradication of P. aeruginosa in CF patients. [Pg.1752]

ACUTE HEALTH RISKS irritation to respiratory tract can overwhelm normal respiratory defense mechanisms and result in temporary difficulty in breathing asbestos splinters may penetrate skin and cause asbestos "corns". [Pg.897]

Sleigh MA. The nature and action of respiratory tract ciUa. In Brain JD, Proctor DF, Reid L, eds. Respiratory Defense Mechanisms. New York Marcel Dekker,... [Pg.92]

The major means by which beryllium enters the body is by the respiratory tract. Since particles greater than 5 )im in diameter will usually be cleared by the mucociliary defense mechanism and either expectorated or swallowed, retention of beryllium is thought to occur only if particles less than 5 xm are inhaled. Particles of less that O.S p.m tend to remain in suspension and are not retained by the lungs. Thus, only particles between 5 and O.S p.m should be retained in the lungs. Both soluble and insoluble forms of beryllium will precipitate when they impact tissue in the distal lower airways. Beryllium appears to be cleared by the lungs in two phases. The first phase is fast with a half-life of several hours to 2 months. The second phase is slow with a half-life from one-half to several years [8-10]. It is probable that once inhalation of beryllium occurs, it is never completely eliminated. [Pg.261]

Preparations containing extracts of the plant Echinacea (family Compositae) are widely used by patients and practitioners in some European countries for preventing and treating upper respiratory tract infections as well as more generally for stimulating the body s own defense mechanisms. At present, about 1000 preparations are obtainable which contain extracts of Echinacea alone or in combination with other plant extracts [1]. In 1993 German physicians prescribed over 3 million daily doses of the five leading preparations with a cost of 50 million DM [2]. As these preparations are often sold over the counter the actual overall use is probably much more widespread. Despite this frequent use, there is considerable debate about the effectiveness of Echinacea extracts, and doubts have been raised about safety in the (relatively rare) case of parenteral application [3,4]. [Pg.105]

As discussed above, absorption to the systemic circulation from the lungs is also a route of exposure of occupational concern. Pulmonary absorption is influenced by the diffusion factors just described, by the degree of hydration at various levels of the respiratory tract and the water solubility and water reactivity of the chemical, and by the integrity of the respiratory system s defense mechanisms. The mucociliary escalator, for example, provides an efficient capture and removal system for inhaled contaminants unless overwhelmed by the magnitude or frequency of exposure or otherwise compromised (e.g., by disease). [Pg.366]

To develop pneumonia, virulent microorganisms must invade the lung parenchyma, either as the result of a defect in defense mechanisms of the host or by an overwhelming inoculum. The normal human respiratory tract has a variety of defense mechanisms such as anatomic barriers, cough reflex, cell and humoral-mediated immunity, and a dual phagocytic system... [Pg.390]

Several factors could explain the possible association between bronchoscopy and VAP, including the use of large volumes of BAL that impede the clearance of bacteria from the lower respiratory tract and the introduction of nosocomial pathogens into the lower airway by dislodging bacterial aggregates from the endotracheal tube surface. As discussed previously, when bacteria encased in biofilm embolize to different areas of the lung, they may be particularly difficult for host defenses to clear effectively (145,146). These pathogenic mechanisms are theoretical, and prospective cUnical studies are required to evaluate the actual risk of bronchoscopy in ventilated patients. [Pg.71]

Most bacterial nosocomial lower respiratory tract infections occur by aspiration of bacteria that colonize the oropharynx or upper gastrointestinal tract of the child. Both intubation and mechanical ventilation alter or circumvent some of the patient s natural barrier defenses against infection. These interventions allow organisms from the oropharyngeal or upper gastrointestinal tract greater access to the lower respiratory tract. The aspiration of contaminated materials may be obvious or, more commonly, it is subclinical. The normal respiratory flora of children admitted to a hospital consists of both gram-positive and... [Pg.212]

The structural configuration of the nasal and oral passageways markedly restrict the access of large particles to the lower respiratory tract. Under normal circumstances, the filtration system of the upper airway and the mucociliary clearance system of the larger airways protect the lower respiratory infection from bacteria that may be present in the patient s environment or that reside in the upper respiratory tract. Nosocomial pneumonia and tracheitis may occur when the mucociliary and cellular defense mechanisms of the lower respiratory tract are evaded. [Pg.213]

The virus attacks the ciliated respiratory epithelium of the airways, with necrosis of the epithelium. Usually, these changes affect mainly the upper conducting airways, but in severe and fatal cases, they extend down to the level of the terminal bronchioles, and the alveoli become filled with protein-containing edema fiuid, red cells, and desquamated alveolar epithelial cells. Following alveolar epithelial cell necrosis, hyaline membranes are often prominent. With recovery from initial infection, the respiratory epithelium regenerates. During this period, however, the mucociliary defense mechanism is defective, and the respiratory tract is particularly prone to attack by secondary invaders. [Pg.191]

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