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

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.

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

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3557-3557
Author(s):  
Noura Ismail ◽  
Clay B. Marsh ◽  
Melissa Hunter

Abstract Microvesicles (MV) (also know as exosomes) are small membrane-bound vesicles released by numerous cell types that contain proteins, mRNA and microRNA. We found that MV from activated monocytes drove survival and differentiation in naïve cells. We therefore were interested in understanding the content of MV produced by activated mononuclear phagocytes. Purified peripheral blood monocytes were treated in vitro for 24 h with or without the monocyte survival factors, GM-CSF or M-CSF, respectively. Examination of monocytes and macrophages by electron microscopy or culture supernatants by flow cytometry demonstrated that monocytes produced MV, which quantitatively increased upon differentiation. Treatment with GM-CSF resulted in more MV production than M-CSF-treated monocytes. To examine whether MV from differentiated cells induced myeloid maturation, the MV were collected and added to fresh monocytes; only MV derived from GM-CSF treated cells induced differentiation of naïve monocytes into macrophages. We next hypothesized that expression of microRNA contained in the MV modulated differentiation of monocytes. Profiling of MV from GM-CSF and M-CSF derived macrophages revealed only two significantly expressed microRNAs. We found that mir-155 was significantly elevated by two-fold in MV from GM-CSF-treated cells, while mir-340 was significantly increased seven-fold in M-CSF-derived MV. Notably, mir- 223 was the highest expressed microRNA in MV from both GM-CSF and M-CSF-treated cells. Recent data suggest that expression of mir-223 regulates myeloid, granulocytic and osteoclasts differentiation, and has a role in hematopoietic stem cell proliferation. While mir-223 is present in MV from both GM-CSF and M-CSF treated cells, it is possible that the low abundance of MV produce from M-CSF-treated cells resulted in less effective concentration to induce differentiation. In this model, it is also possible that regulation of proteins targeted by the increase in mir-155 and decrease mir-340 in the GM-CSF-derived MV are responsible for myeloid differentiation. Since changes in microRNA expression including mir-223 has been reported in AML, our data suggest that myeloid-derived MV in the peripheral blood containing mir-223 may be altered contributing to leukemogenesis.


2020 ◽  
Vol 11 (4) ◽  
pp. 494-500
Author(s):  
O. M. Koliada ◽  
N. I. Vdovichenko ◽  
T. I. Kolyada ◽  
O. P. Bilozorov

Functional and metabolic features of intact and stimulated mononuclear phagocytes were studied in patients with different clinical courses of multiple sclerosis, the study included 66 patients with relapsing-remitting and 32 patients with progressive course of multiple sclerosis. The state of the mononuclear phagocytes was characterized by expression of costimulatory molecules and direction of L-arginine metabolism. Relative quantities of CD80, CD86 and PD-L1 positive monocytes were determined with Phycoerytrin-labeled monoclonal antibodies in immunofluorescence test in peripheral blood and after culture in parallel series with addition of: (a) E.coli lipopolysaccharide (a stimulator of TLR4), (b) a single-stranded RNA – preparation ssRNA40/LyoVec (a stimulator of TLR7/8), (c) IL-4 (an anti-inflammatory interleukin). The formation of NO was determined by the amount of nitrite in the culture supernatants, arginase activity was determined in cell lysates of the monocyte fraction. We showed that functional and phenotypic characteristics of monocytes depend on the clinical course of multiple sclerosis. In patients with progressive course, the relative number of CD86+ cells was significantly higher and PD-L1+ cells significantly lower than in patients with relapsing-remitting course and healthy persons, in patients with relapsing-remitting course the number of PD-L1+ cells was increased. The number of CD80+ cells did not show any significant difference in the investigated groups of patients relative to the control group. In vitro stimulation of peripheral blood monocytes with TLR4/8 produced a significant increase in the number of CD86+ and decrease in the number of PD-L1+ cells in patients with the progressive course. In patients with the relapsing-remitting course LPS produced an increase in number of PD-L1+ cells. We did not find any difference in activity of the arginase pathway of L-arginine metabolism in the intact monocyte fraction of peripheral blood in patients with multiple sclerosis versus the control group, but stimulation with TLR4 agonist of mononuclear cells of patients with progressive course caused significant increased arginase activity versus baseline. At the same time, versus control cells arginase activity in patients with the progressive course decreased after LPS treatment, but trended to increase after TLR7/8 treatment. In patients with the relapsing-remitting course these changes had a similar direction but were less expressed. The results may be considered as an indication of the activation of peripheral blood monocytes and their polarization trend in the M1 direction in patients with the progressive course of multiple sclerosis, these changes could be considered as signs of violation of autoimmune regulatory mechanisms in multiple sclerosis.


1990 ◽  
Vol 68 (6) ◽  
pp. 2384-2390 ◽  
Author(s):  
V. Mohsenin ◽  
J. Latifpour

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)


AIDS ◽  
1998 ◽  
Vol 12 (7) ◽  
pp. 719-727 ◽  
Author(s):  
Sharon R. Lewin ◽  
Jean Kirihara ◽  
Secondo Sonza ◽  
Lou Irving ◽  
John Mills ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document