Dust and LPS Induced Stimulation of Nitrite and Nitrate Release in Bovine Alveolar Macrophages

1992 ◽  
pp. 231-234
Author(s):  
T. Schlüter ◽  
I. Berg ◽  
G. Gercken
Keyword(s):  
Alveolar Macrophages ◽  
Stimulation Of

Different pathways of degradation of SP-A and saturated phosphatidylcholine by alveolar macrophages

2000 ◽  
Vol 279 (1) ◽  
pp. L91-L99 ◽  
Author(s):  
Aldo Baritussio ◽  
Antonella Alberti ◽  
Decio Armanini ◽  
Federica Meloni ◽  
Daniela Bruttomesso
Keyword(s):  
Plasma Membrane ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Alveolar Macrophages ◽  
Surfactant Protein ◽  
Phosphatidylinositol 3 Kinase ◽  
Lysosomal Compartment ◽  
Lysosomal Ph ◽  
Kinase C ◽  
Stimulation Of

Alveolar macrophages degrade surfactant protein (SP) A and saturated phosphatidycholine [dipalmitoylphosphatidylcholine (DPPC)]. To clarify this process, using rabbit alveolar macrophages, we analyzed the effect of drugs known to affect phagocytosis, pinocytosis, clathrin-mediated uptake, caveolae, the cytoskeleton, lysosomal pH, protein kinase C, and phosphatidylinositol 3-kinase (PI3K) on the degradation of SP-A and DPPC. We found the following: 1) SP-A binds to the plasma membrane, is rapidly internalized, and then moves toward degradative compartments. Uptake could be clathrin mediated, whereas phagocytosis, pinocytosis, or the use of caveolae are less likely. An intact cytoskeleton and an acidic milieu are necessary for the degradation of SP-A. 2) Stimulation of protein kinase C increases the degradation of SP-A. 3) PI3K influences the degradation of SP-A by regulating both the speed of internalization and subsequent intracellular steps, but its inhibition does not prevent SP-A from reaching the lysosomal compartment. 4) The degradation of DPPC is unaffected by most of the treatments able to influence the degradation of SP-A. Thus it appears that DPPC is degraded by alveolar macrophages through mechanisms very different from those utilized for the degradation of SP-A.

Stimulation of oxidant production in alveolar macrophages by pollutant and latex particles

1980 ◽  
Vol 23 (1) ◽  
pp. 121-136 ◽  
Author(s):  
Gary E. Hatch ◽  
Donald E. Gardner ◽  
Daniel B. Menzel
Keyword(s):  
Alveolar Macrophages ◽  
Latex Particles ◽  
Oxidant Production ◽  
Stimulation Of

scholarly journals Rat surfactant protein D enhances the production of oxygen radicals by rat alveolar macrophages

1992 ◽  
Vol 286 (1) ◽  
pp. 5-8 ◽  
Author(s):  
J F Van Iwaarden ◽  
H Shimizu ◽  
P H M Van Golde ◽  
D R Voelker ◽  
L M G Van Golde
Keyword(s):  
Alveolar Macrophages ◽  
Oxygen Radicals ◽  
Protein A ◽  
Surfactant Protein ◽  
Surfactant Protein A ◽  
Surfactant Protein D ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Oxygen Radical Production ◽  
Stimulation Of

Rat surfactant protein D (SP-D) was shown to enhance the production of oxygen radicals by rat alveolar macrophages. This enhancement, which was determined by a lucigenin-dependent chemiluminescence assay, was maximal after 18 min at an SP-D concentration of 0.2 micrograms/ml. Surfactant lipids did not influence the stimulation of alveolar macrophages by SP-D, whereas the oxygen-radical production of these cells induced by surfactant protein A was inhibited by the lipids in a concentration-dependent manner.

Exposure to ambient particles accelerates monocyte release from bone marrow in atherosclerotic rabbits

2004 ◽  
Vol 287 (1) ◽  
pp. L79-L85 ◽  
Author(s):  
Yukinobu Goto ◽  
James C. Hogg ◽  
Chih-Horng Shih ◽  
Hiroshi Ishii ◽  
Renaud Vincent ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Transit Time ◽  
Alveolar Macrophages ◽  
Ambient Particles ◽  
Cell Counts ◽  
Thymidine Analog ◽  
Rapid Release ◽  
Dividing Cells ◽  
Progression Of Atherosclerosis ◽  
Stimulation Of

Exposure to air pollution [particulate matter, particles <10 μm (PM10)] causes a systemic inflammatory response that includes stimulation of the bone marrow (BM) and progression of atherosclerosis. Monocytes are known to play a key role in atherogenesis by migration into subendothelial lesions where they appear as foam cells. The present study was designed to quantify the BM monocyte response in Watanabe heritable hyperlipidemic (WHHL) rabbits after PM10exposure. WHHL rabbits were given twice weekly intrapharyngeal instillations of 5 mg of PM10for 4 wk to a total of 40 mg and compared with control WHHL or New Zealand White (NZW) rabbits. The thymidine analog 5′-bromo-2′-deoxyuridine was used to label dividing cells in the BM and a monoclonal antibody to identify monocytes in peripheral blood. The transit time of monocytes through the BM was faster in WHHL than in NZW rabbits (30.4 ± 1.9 h vs. 35.2 ± 0.9 h, WHHL vs. NZW; P < 0.05). PM10instillation exposure increased circulating band cell counts, caused rapid release of monocytes from the BM, and further shortened their transit time through the BM to 23.2 ± 1.6 h ( P < 0.05). The percentage of alveolar macrophages containing particles in the lung correlated with the BM transit time of monocytes (r2= 0.45, P <0.05). We conclude that atherosclerosis increases the release of monocytes from the BM, and PM10exposure accelerates this process in relation to the amount of particles phagocytosed by alveolar macrophages.

Stimulation of Arachidonic Acid Metabolism in Silica-Exposed Alveolar Macrophages

1989 ◽  
Vol 15 (4) ◽  
pp. 511-526 ◽  
Author(s):  
Mark D. Englen ◽  
Stephen M. Taylor ◽  
William W. Laegreid ◽  
H. Denny Liggitt ◽  
Ron M. Silflow ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Alveolar Macrophages ◽  
Acid Metabolism ◽  
Arachidonic Acid Metabolism ◽  
Stimulation Of
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