Proliferation activity and bacteriostatic potential of human blood monocytes, macrophages in pleural effusions, ascites, and of alveolar macrophages

Abstract

Human blood monocytes, macrophages from pleural effusions, ascites, and alveolar macrophages obtained by bronchopulmonary lavage were investigated. The proliferative activity of these cells was determined by the 3H-thymidine labeling index in vitro (3H-TDR L.I.). The bacteriostatic capacity was measured by the potential of the cells to block DNA-synthesis of proliferating Escherichia coli after phagocytosis. In most cases 3H-TDR L.I. of blood monocytes, macrophages from pleural effusions and ascites was less than 1%. However, macrophages of some patients with neoplastic diseases exhibited 3H-TDR L.I. between 4.0--9.6%. This probably reflected the action of factors, possibly lymphokines, which stimulated macrophage proliferation. In contrast, alveolar macrophages seemed to have almost totally lost their proliferative potential. The bacteriostatic capacity of blood monocytes proved to be significantly lower than that of macrophages. This demonstrates the functional immaturity of blood monocytes. In all type of macrophages investigated the bacteriostatic power was very high. No differences could be detected either between macrophages of different sources or between macrophages of benign, inflammatory, or malignant diseases.

Pleural macrophages are the dominant cell population in the thoracic cavity with an inflammatory cytokine profile similar to peritoneal macrophages

“…Data on the pleural lavage cytology are mainly derived from pathological effusion in tumor patients [14,15]. Limited information is available about the cellular composition of the pleural cavity in healthy humans.…”

Pulmonary Macrophages

“…Elastases, collagenases, and various other proteolytic enzymes have also been identified in lysosomal vesicles, many of which are secreted externally (Harris et al, 1975;Rouzer et al, 1982;Bowden, 1984;du Bois, 1985;Bilyk et al, 1988;Lehnert et al, 1990). Flow cytometric analysis has shown that murine alveolar macrophages are unique, relative to macrophages in other tissues, in that they express high levels of CD11c or integrin alpha X (Taylor et al, 2000;Lagranderie et al, 2003; Meuret et al, 1980;Lehnert et al, 1988;Chitko-McKown et al, 1991;Lehnert, 1992;Peao et al, 1992;Staub, 1994;Longworth, 1997;Gjomarkaj et al, 1999;Frankenberger et al, 2000;Zetterberg et al, 2000;Fathi et al, 2001;Lagranderie et al, 2003;Grundy and Sentman, 2005 Chemotaxis þ þ þ Holt et al, 1982;Prokhorova et al, 1994;Wizemann and Laskin, 1994b;Steinmuller et al, 2000 Cytotoxicity þþþ þ þþþþ Chitko-McKown et al, 1991;Staub, 1994;Longworth, 1997;Gjomarkaj et al, 1999;Steinmuller et al, 2000 Dendritic cell suppression þ þþþ Bedoret et al, 2009 Antigen presentation þ þþþ þþ þ Miller et al, 1992;Gjomarkaj et al, 1999;Zetterberg et al, 2000;Lay et al, 2009 Modulate T cell proliferation þ þþþ þþ þþþ Holt, 1979a;Holt et al,...…”

Alveolar macrophage replication. One mechanism for the expansion of the mononuclear phagocyte population in the chronically inflamed lung.

“…These findings suggest that replication within the alveolar structures may account, in part, for the expansion of the population of mononuclear phagocytes observed in chronic inflammatory disorders. (46) and in chronic exudates in the pleural (47) and peritoneal cavities (48). Moreover, several studies have shown that bovine (49), murine (50), and hamster (45) (18)(19)(20)(21)(22)(23)(24).…”