The role of extracellular bactericidal factors in pulmonary host defense.
Extracellular killing provides an attractive hypothesis to explain the rapid alveolar killing of inhaled bacterial pathogens in the absence of conventional opsonins for phagocytosis. Some evidence of extracellular killing of inhaled pneumococci has been obtained using histologic studies and bronchoalveolar lavage. Although studies of the antimicrobial activity of lung lavage fluid in vitro have given variable results, a variety of antimicrobial factors have been detected in lung lavage fluids. Studies of lysozyme, peptides, iron binding proteins, free fatty acids and other factors that are found free in lung lavage fluid indicate that some of these factors could be a part of extracellular pulmonary host defenses. However, their precise role is not known. A survey of mechanisms of extracellular killing shows that granulocytes, monocytes, macrophages, and T lymphocytes all have the capacity to kill extracellularly in vitro in some circumstances. It remains to be determined which of these diverse mechanisms operate within the lung and how they function in relationship to other host defenses.
Coonrod
J D
JD
Veterans Administration, Lexington, Ky.
D000818:Animals; D001424:Bacterial Infections / Q000276:immunology*; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D005230:Fatty Acids, Nonesterified / Q000276:immunology; D006801:Humans; D007781:Lactoferrin / Q000276:immunology; D007962:Leukocytes / Q000276:immunology; D008168:Lung / Q000276:immunology*; D009113:Muramidase / Q000276:immunology; D010196:Pancreatic Elastase / Q000276:immunology; D010455:Peptides / Q000276:immunology; D010587:Phagocytosis; D011650:Pulmonary Alveoli / Q000276:immunology; D011663:Pulmonary Surfactants / Q000276:immunology; D014168:Transferrin / Q000276:immunology
D005230:Fatty Acids, Nonesterified; D010455:Peptides; D011663:Pulmonary Surfactants; D014168:Transferrin; D009113:Muramidase; D007781:Lactoferrin; D010196:Pancreatic Elastase