The lung mast cell: Its physiology and potential relevance to defense of the lung

Abstract

The mast cell, located at mucosal surfaces and surrounding venules, is uniquely positioned to respond rapidly to insults to the host by mediating the development of a wide-ranging inflammatory response. Activation of the mast cell releases preformed granule-associated chemical mediators and generates de novo biologically active materials. The properties of the mast cell mediators permit development of both acute and prolonged inflammatory responses. The immediate response is characterized by edema and the delayed response by leukocyte infiltration and vascular damage. The mast cell mediators responsible for these inflammatory events are characterized functionally. The vasoactive/smooth muscle reactive mediators include preformed histamine and serotonin and newly-generated platelet activating factor, slow reacting substance of anaphylaxis and prostaglandins. Chemotactic mediators include eosinophil-selective ECF-A and ECF-oligopeptides, neutrophil-selective NCF, and lipid chemotactic mediators with broad specificity. These factors induce directed migration and localization of leukocytes. The mast cell releases the structural proteoglycan, heparin, which is anticoagulant and inhibits complement. Released mast cell enzymes include chymotryptic and tryptic proteases, arylsulfatase, β-glucoronidase, and hexosaminidase. The proteolytic enzymes may activate inflammatory pathways while the others degrade ground substance. The capacity of the mast cell to enhance vascular permeability, to cause the influx of regulatory or inflammatory leukocytes, and to provide a variety of active enzymes permits regulation of inflammatory events at the site of tissue injury.