scholarly journals Proteomic and bioinformatics profile of paired human alveolar macrophages and peripheral blood monocytes

PROTEOMICS ◽  
2015 ◽  
Vol 15 (22) ◽  
pp. 3797-3805 ◽  
Author(s):  
Sara E. Tomechko ◽  
Kathleen C. Lundberg ◽  
Jessica Jarvela ◽  
Gurkan Bebek ◽  
Nicole G. Chesnokov ◽  
...  
Keyword(s):  
Alveolar Macrophages ◽  
Peripheral Blood ◽  
Blood Monocytes ◽  
Peripheral Blood Monocytes ◽  
Human Alveolar Macrophages

Surfactant proteins A and D specifically stimulate directed actin-based responses in alveolar macrophages

1999 ◽  
Vol 276 (1) ◽  
pp. L164-L174 ◽  
Author(s):  
Michael James Tino ◽  
Jo Rae Wright
Keyword(s):  
Alveolar Macrophages ◽  
Peripheral Blood ◽  
Actin Polymerization ◽  
Cell Types ◽  
Surfactant Protein ◽  
Mononuclear Phagocytes ◽  
Blood Monocytes ◽  
Cellular Functions ◽  
Peripheral Blood Monocytes ◽  
Specific Effects

Surfactant protein (SP) A and SP-D are the pulmonary members of the collectin family, structurally related proteins involved in innate immune responses. Here, we have examined the abilities of SP-A, SP-D, mannose-binding protein (MBP), and the complement component C1q to stimulate actin-based cellular functions in rat alveolar macrophages and peripheral blood monocytes. Our goal in this study was to examine the cell specificity of the effects of the collectins to understand further the mechanisms by which SP-A and SP-D stimulate alveolar macrophages. We found that SP-A and SP-D have lung cell-specific effects at physiologically relevant concentrations; they stimulate directional actin polymerization and chemotaxis in alveolar macrophages but not in monocytes. Although C1q and MBP weakly stimulate the rearrangement of actin in both cell types, C1q is chemotactic only for peripheral blood monocytes and MBP does not stimulate chemotaxis of either cell type. Neither C1q nor MBP stimulates actin polymerization in alveolar macrophages. These results support the hypothesis that alveolar macrophages express receptors specific for the pulmonary collectins SP-A and SP-D and provide insight into the potential roles of collectins in the recruitment and maturation of mononuclear phagocytes in the lung.

Respiratory burst in alveolar macrophages of diabetic rats

1990 ◽  
Vol 68 (6) ◽  
pp. 2384-2390 ◽  
Author(s):  
V. Mohsenin ◽  
J. Latifpour
Keyword(s):  
Alveolar Macrophages ◽  
Respiratory Burst ◽  
Peripheral Blood ◽  
Diabetic Rats ◽  
Blood Monocytes ◽  
Peripheral Blood Monocytes ◽  
Significant Difference ◽  
Cytochrome C Reduction ◽  
Generating Capacity ◽  
O2 Production

Bactericidal ability of alveolar macrophages is depressed in rats with diabetes mellitus. To define the mechanism of this abnormality, we measured the parameters of respiratory burst in alveolar macrophages, peripheral blood monocytes, and neutrophils of rats 8 wk after the induction of diabetes by streptozocin. Superoxide anion (O2-.) generation during basal conditions and after stimulation with phorbol myristate acetate (PMA) was measured as superoxide dismutase-inhibitable cytochrome c reduction. NADPH, the principal substrate for NADPH-oxidase-dependent O2-. generation, was measured in the alveolar macrophages and quick-frozen lungs by the enzyme-cycling method. O2-. generation after PMA was significantly lower in the alveolar macrophages of diabetics than in the controls (14.4 +/- 2.0 nmol.10(6) cells-1.20 min-1 vs. 26.2 +/- 1.9, P less than 0.05). Conversely the peripheral blood monocytes of diabetics demonstrated an enhanced O2-. production after PMA stimulation. There was no significant difference in the neutrophil O2-.-generation between the groups. The alveolar macrophage NADPH (control 0.44 +/- 0.15 nmol/10(6) cells vs. diabetic 0.21 +/- 0.04, P less than 0.05) and lung tissue NADPH levels (control 81.4 +/- 16.3 nmol/g dry wt vs. diabetic 35.8 +/- 20.5, P less than 0.05) were significantly lower in the diabetics than in the controls. These data indicate that the O2-.-generating capacity of alveolar macrophages is markedly depressed in diabetes, whereas their precursors, monocytes, are primed to generate O2-. with PMA stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

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