Host-pathogen relationships in respiratory tract infections.
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)
Verhoef
J
J
Department of Clinical Microbiology and Infectious Diseases, University Hospital Utrecht, The Netherlands.
D001419:Bacteria / Q000472:pathogenicity; D001424:Bacterial Infections / Q000382:microbiology / Q000503:physiopathology*; D006801:Humans; D008264:Macrophages / Q000502:physiology*; D009504:Neutrophils / Q000502:physiology*; D010587:Phagocytosis / Q000502:physiology; D012141:Respiratory Tract Infections / Q000382:microbiology / Q000503:physiopathology*; D014774:Virulence