title: Pulmonary intravascular macrophages. Role in acute lung injury.
abstract: PIMs, although present only in selected animal species, may provide a clue to the potential role of mononuclear phagocytes on the vascular side of the air-blood barrier in lung inflammation and injury. We know PIMs localize circulating pathogens to the lungs in animals and concentrate the inflammatory response in the lung parenchyma. In certain disease states-e.g., biliary cirrhosis-pulmonary phagocytes may develop in the pulmonary capillaries, placing the lungs at risk for pathogen localization and subsequent inflammation. The two experimental approaches described last in this article-induction of intravascular macrophages in the lungs of rodents or rabbits and the selective inhibition or destruction of PIMs-offer models to study the role of mononuclear phagocytes in lung injury. The cirrhotic rat, especially, offers a model to investigate the interaction between pulmonary phagocytes and liver disease, including the adhesive molecules necessary for monocytes to adhere and differentiate in pulmonary capillaries. We then can investigate whether such factors arise in human lungs. We now can determine selectively whether macrophages can cause lung injury and what mediators they may contribute to the complex interactions among inflammatory cells, cytokines, proteases, oxygen radicals, and lipid mediators that participate in early sepsis-induced lung injury.
authors.affiliation: Center for Animal Resources and Comparative Medicine, Harvard Medical School, Boston, Massachusetts, USA.
authors.forename: A E
authors.initials: AE
authors.lastname: Warner
mesh_terms: D000818:Animals; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology; D008103:Liver Cirrhosis / Q000503:physiopathology; D008107:Liver Diseases / Q000473:pathology / Q000503:physiopathology*; D008168:Lung / Q000166:cytology / Q000502:physiology; D008171:Lung Diseases / Q000473:pathology / Q000503:physiopathology*; D016676:Macrophages, Alveolar / Q000473:pathology / Q000502:physiology; D018805:Sepsis / Q000503:physiopathology
chemical_list: D018836:Inflammation Mediators