Origin and kinetics of pulmonary macrophages during an inflammatory reaction induced by intravenous administration of heat-killed bacillus Calmette-Guérin.

Abstract

The main defenders of the respiratory organs against microorganisms and other foreign substances are the pulmonary macrophages. The majority of these cells, which belong to the mononuclear phagocyte system (1), are normally located in the alveolar spaces, where they phagocytize surfactants (2) and various substances introduced via the airways ; the remainder occur in the interstitial lung tissue (3) . The origin and kinetics of the pulmonary macrophages have been controversial, mostly because of differences in the interpretation of DNA-labeling characteristics in the absence of accurate quantitative information. Recently, a method developed to study the total pulmonary macrophage population by optimal lavage of the airways followed by enzyme digestion of lavaged lung tissue after removal of circulating monocytes from the pulmonary blood vessels enabled us to demonstrate that the great majority of the pulmonary macrophages of mice in the normal steady state derive from circulating monocytes originating in the bone marrow (4), and that local proliferation of mononuclear phagocytes does not play a significant role in the maintenance of the pulmonary macrophage population . ' The origin and kinetics of the increased number of pulmonary macrophages during acute inflammatory reactions are, however, still a matter of debate . On the basis of studies done of inflammation induced by various stimuli ranging from inert particles to pathogenic microorganisms and noxious gases in various animal models, both an influx of circulating monocytes and interstitial multiplication of macrophages or macrophage-precursor cells have been claimed to contribute to the pulmonary macrophage population under these conditions (5-9) .The present report concerns the macrophage kinetics during an inflammatory reaction in the lungs after the intravenous injection of heat-killed bacillus CalmetteGuerin (BCG).2 The kinetic patterns were studied by following the course and determining the DNA-labeling characteristics of both the circulating monocytes and the total macrophage population, i.e., the alveolar and interstitial macrophages. 2 Abbreviatons used in this paper. AML, alveolar-macrophage-like ; BCC, bacillus Calmette-Guerin ; C, complement ; HC, hydrocortisone acetate; NAML, non-alveolar-macrophage-like ; t DNA-synthesis time; ZN, Ziehl-Neelsen . J . Exp . MED .

Lung interstitial macrophages alter dendritic cell functions to prevent airway allergy in mice

“…By contrast, our data unambiguously demonstrate that IMs are capable of preventing LPS-triggered Th2 priming through functional inhibition of lung DCs. Taken together, our results indicate that IMs are not merely the precursors of AMs as previously proposed by Blussé van Oud Alblas et al (40), but constitute a phenotypically and functionally distinct macrophage population that contributes to the fine-tuning of respiratory immune responses. Determining their ontological relation with AMs will require additional investigation.…”

Characterization and quantification of alveolar monocyte-like cells in human chronic inflammatory lung disease

“…Further animal studies have demonstrated that the increase of the pulmonary macrophage population during an acute inflammation is brought about mainly by monocyte influx and to a minor extent by temporarily increased local production of macrophages [9]. Consequently, the appearance of small monocyte-like AMs was described in further experimental studies both of acute [32] and chronic [22] lung inflammation.…”

“…Under noninflammatory conditions, AMs are thought to be maintained both by local proliferation of resident pulmonary macrophages and extravasation of circulating, bone marrow-derived monocytes [6,7]. In lung inflammation, however, it has been suggested that increased numbers of monocytes extravasate from the pulmonary microvasculature to the bronchoalveolar space [8,9].…”

Accessory cells with immunophenotypic and functional features of monocyte-derived dendritic cells are recruited to the lung during pulmonary inflammation

“…Exudate Ms in the inflamed lung are accounted for primarily by the recruitment of circulating monocyte precursors [3,4]. Recent evidence suggests that blood monocytes cultured with granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin (IL-4) in vitro develop features of dendritic cells (DC) [5][6][7].…”