Host-pathogen relationships in respiratory tract infections
- PMID: 2029721
Host-pathogen relationships in respiratory tract infections
Abstract
The respiratory tract is continuously exposed to inhaled particles. The mucous membrane and the mechanisms of sneezing, coughing, and mucociliary clearance are the first line of defense. For the bronchioli and alveoli, the phagocytic cells are the cornerstone of defense against invading microorganisms. Alveolar macrophages and polymorphonuclear leukocytes are responsible for phagocytosis. For optimal phagocytosis, antibodies and complement are needed; phagocytic cells possess receptors for the Fc fragment of the immunoglobulin (IgG) molecule and complement. Receptors for cytokines are also present. These cytokines are important for activating the alveolar macrophage and recruiting other phagocytic cells and lymphocytes to the site of infection. Alveolar macrophages also contain cytophilic antibodies, IgG molecules that are bound to the cell via the F(ab)2 fragments. These cytophilic antibodies can interfere with the process of phagocytosis. They can bind to bacteria containing an Fc receptor (eg, Staphylococcus aureus protein A) and therefore provide the alveolar macrophage with a means to bind and digest staphylococci. Pulmonary surfactant proteins enhance the uptake of bacteria and viruses by alveolar macrophages and viruses. Thus surfactant contributes to the defense mechanisms of the lung. Phagocytic cells can injure alveoli. During the process of phagocytosis, toxic oxygen species and enzymes, needed for killing bacteria, are produced. These toxic substances may leak out of the cell and damage the surrounding tissues. All these phenomena contribute to the processes of inflammation. The function of phagocytic cells is decreased in smokers and by certain air pollutants. Phagocytic cells are crucial for the elimination of microorganisms.(ABSTRACT TRUNCATED AT 250 WORDS)
Similar articles
-
Role of the alveolar macrophage in pulmonary bacterial defense.Bull Eur Physiopathol Respir. 1977 Jan-Feb;13(1):57-67. Bull Eur Physiopathol Respir. 1977. PMID: 321054 Review.
-
Phagocytic defense in the lung.Antibiot Chemother (1971). 1985;36:74-87. Antibiot Chemother (1971). 1985. PMID: 3890719 Review.
-
Host defense impairments that may lead to respiratory infections.Clin Chest Med. 1987 Sep;8(3):339-58. Clin Chest Med. 1987. PMID: 3311580 Review.
-
[Phagocytic defense against bacterial infection: a new in vitro experimental model. Alveolar macrophages].Bull Int Union Tuberc. 1976;51(1 Pt 2):541-50. Bull Int Union Tuberc. 1976. PMID: 1052899 French. No abstract available.
-
Pulmonary defense mechanisms and the interaction between viruses and bacteria in acute respiratory infections.Bull Eur Physiopathol Respir. 1977 Jan-Feb;13(1):119-35. Bull Eur Physiopathol Respir. 1977. PMID: 321050 Review.
Cited by
-
A Pseudomonas aeruginosa toxin that hijacks the host ubiquitin proteolytic system.PLoS Pathog. 2011 Mar;7(3):e1001325. doi: 10.1371/journal.ppat.1001325. Epub 2011 Mar 24. PLoS Pathog. 2011. PMID: 21455491 Free PMC article.
-
Pathogenesis of tuberculosis: interaction of Mycobacterium tuberculosis with macrophages.Infect Immun. 1993 Jul;61(7):2763-73. doi: 10.1128/iai.61.7.2763-2773.1993. Infect Immun. 1993. PMID: 8514378 Free PMC article.
Publication types
MeSH terms
LinkOut - more resources
Medical