Interleukin 1 release by human alveolar macrophages and blood monocytes

1989 ◽  
Vol 256 (5) ◽  
pp. C1012-C1015 ◽  
Author(s):  
G. K. Iwamoto ◽  
M. M. Monick ◽  
L. F. Burmeister ◽  
G. W. Hunninghake
Keyword(s):  
Prostaglandin E2 ◽  
Alveolar Macrophages ◽  
Interleukin 1 ◽  
Cell Types ◽  
Interleukin 1 Beta ◽  
Blood Monocytes ◽  
Time Points ◽  
Specific Radioimmunoassay ◽  
Human Alveolar Macrophages

These studies utilized a sensitive and specific radioimmunoassay for interleukin 1 beta (IL-1 beta) to compare release of IL-1 by human alveolar macrophages and blood monocytes. The studies demonstrate that alveolar macrophages release amounts of antigenic IL-1 beta that are similar to that of blood monocytes. The amounts of IL-1 released were similar for both cell types at early (4 h) and late (24 h) time points and with differing amounts of stimuli [endotoxin; lipopolysaccharide (LPS)]. In addition, alveolar macrophages actually produced more total IL-1 (intracellular IL-1 plus released IL-1) than did blood monocytes. Alveolar macrophages that were stimulated with LPS released significantly more prostaglandin E2 (PGE2, an inhibitor of IL-1) than did blood monocytes. These studies demonstrate that human alveolar macrophages are not defective in their capacity to release IL-1.

Cigarette smoking decreases interleukin 1 release by human alveolar macrophages

1989 ◽  
Vol 256 (2) ◽  
pp. C260-C264 ◽  
Author(s):  
G. P. Brown ◽  
G. K. Iwamoto ◽  
M. M. Monick ◽  
G. W. Hunninghake
Keyword(s):  
Lactate Dehydrogenase ◽  
Alveolar Macrophages ◽  
Interleukin 1 ◽  
Smoking History ◽  
Interleukin 1 Beta ◽  
Lactate Dehydrogenase Release ◽  
Wide Range ◽  
Human Alveolar Macrophages ◽  
Pge2 Release ◽  
Heavy Smokers

To determine whether alveolar macrophages from smokers have an abnormal interleukin 1 beta (IL-1) release, we obtained macrophages by bronchoalveolar lavage (BAL) of otherwise healthy volunteers in three groups: nonsmokers (NS; n = 11), light smokers (LS, less than 10 pack-yr smoking history; n = 4) and heavy smokers (HS, greater than 10 pack-yr smoking history; n = 9). After 24 h in culture, unstimulated macrophages (from each group) released negligible amounts of IL-1. Lipopolysaccharide (LPS) (1 micrograms/ml) caused release of 21.77 +/- 4.33 ng IL-1/10(6) cells at 24 h from NS macrophages; IL-1 release from HS macrophages was significantly decreased (5.52 +/- 1.66 ng/10(6) cells; P less than 0.05), whereas LS macrophages released intermediate amounts (15.07 +/- 6.15 ng/10(6) cells). Release of IL-1 from HS macrophages was also decreased after 48 and 72 h in culture and was observed over a wide range of concentrations of LPS. The decreased amount of IL-1 in HS macrophage supernatants appeared to be due to a defect in release of IL-1 from the cells and not due to a defect in production of the mediator, since total IL-1 (IL-1 present in the cell lysates plus that in the cell supernatants) was similar in the NS and HS groups. In addition, after 24 h in culture, LPS-stimulated HS macrophages released significantly less prostaglandin E2 (PGE2) (which can suppress IL-1 production) than did NS macrophages; in the presence of indomethacin, which abolished macrophage PGE2 release, no augmentation of LPS-stimulated IL-1 release was observed. Cell viability, as measured by lactate dehydrogenase release, was not different between HS and NS macrophages under any conditions. We conclude that there is a defect in release but not production of IL-1 from the alveolar macrophages of chronic smokers.

IL-1 receptor antagonist release is regulated differently in human alveolar macrophages than in monocytes

1992 ◽  
Vol 73 (4) ◽  
pp. 1686-1692 ◽  
Author(s):  
J. N. Kline ◽  
M. M. Monick ◽  
G. W. Hunninghake
Keyword(s):  
Receptor Antagonist ◽  
Alveolar Macrophages ◽  
Interleukin 1 ◽  
Calf Serum ◽  
Cell Types ◽  
Cell Group ◽  
Blood Monocytes ◽  
Gm Csf ◽  
Monocytes And Macrophages ◽  
Macrophage Colony

These studies compared the release of interleukin-1 receptor antagonist (IL-1 RA) from alveolar macrophages and peripheral blood monocytes. The cells were cultured in medium containing various amounts of heat-inactivated fetal calf serum (FCS), granulocyte-macrophage colony-stimulating factor (GM-CSF), lipopolysaccharide (LPS), and immunoglobulin G (IgG). In serum-free medium alone, IL-1 RA release was similar from macrophages and monocytes. Increasing FCS concentration caused a significant upregulation of IL-1 RA release in macrophages but not in monocytes. GM-CSF caused a small increase in both cell types. LPS caused downregulation of IL-1 RA release from monocytes but not from macrophages. IgG did not affect IL-1 RA release in either cell group. These studies demonstrate that regulation of IL-1 RA release is different in monocytes and macrophages.

Toward functional proteomics of alveolar macrophages

2005 ◽  
Vol 288 (4) ◽  
pp. L585-L595 ◽  
Author(s):  
Haifeng M. Wu ◽  
Ming Jin ◽  
Clay B. Marsh
Keyword(s):  
Alveolar Macrophages ◽  
Large Scale ◽  
Cell Types ◽  
Mononuclear Phagocyte ◽  
Detection Sensitivity ◽  
Current Status ◽  
Blood Monocytes ◽  
Protein Patterns ◽  
Additional Information ◽  
The Impact

Alveolar macrophages (AM) belong to a phenotype of macrophages with distinct biological functions and important pathophysiological roles in lung health and disease. The molecular details determining AM differentiation from blood monocytes and AM roles in lung homeostasis are largely unknown. With the use of different technological platforms, advances in the field of proteomics have made it possible to search for differences in protein expression between AM and their precursor monocytes. Proteome features of each cell type provide new clues into understanding mononuclear phagocyte biology. In-depth analyses using subproteomics and subcellular proteomics offer additional information by providing greater protein resolution and detection sensitivity. With the use of proteomic techniques, large-scale mapping of phosphorylation differences between the cell types have become possible. Furthermore, two-dimensional gel proteomics can detect germline protein variants and evaluate the impact of protein polymorphisms on an individual's susceptibility to disease. Finally, surface-enhanced laser desorption and ionization (SELDI) time-of-flight mass spectrometry offers an alternative method to recognizing differences in protein patterns between AM and monocytes or between AM under different pathological conditions. This review details the current status of this field and outlines future directions in functional proteomic analyses of AM and monocytes. Furthermore, this review presents viewpoints of integrating proteomics with translational topics in lung diseases to define the mechanisms of disease and to uncover new diagnostic and therapeutic targets.

scholarly journals Febrile responses induced in adrenalectomized rats by administration of interleukin-1 beta or prostaglandin E2.

1995 ◽  
Vol 484 (3) ◽  
pp. 767-775 ◽  
Author(s):  
T Watanabe ◽  
T Makisumi ◽  
M Macari ◽  
N Tan ◽  
T Nakamori ◽  
...  
Keyword(s):  
Prostaglandin E2 ◽  
Interleukin 1 ◽  
Interleukin 1 Beta ◽  
Adrenalectomized Rats

Is the Success of Cefazolin plus Ertapenem in Methicillin-Susceptible Staphylococcus aureus Bacteremia Based on Release of Interleukin 1-beta?

2022 ◽  
Author(s):  
Dan Smelter ◽  
Mary Hayney ◽  
George Sakoulas ◽  
Warren Rose
Keyword(s):  
Staphylococcus Aureus ◽  
Peripheral Blood ◽  
Interleukin 1 ◽  
Interleukin 1 Beta ◽  
Blood Monocytes ◽  
Salvage Regimen ◽  
Peripheral Blood Monocytes ◽  
Staphylococcus Aureus Bacteremia

Cefazolin and ertapenem has been shown to be an effective salvage regimen for refractory methicillin-susceptible Staphylococcus aureus bacteremia. Our findings suggest cefazolin plus ertapenem in vitro stimulates interleukin-1β release from peripheral blood monocytes both with and without S. aureus presence. This IL-1β augmentation was primarily driven by ertapenem. These findings support further exploration of cefazolin plus ertapenem in MSSA bacteremia and may partially explain its marked potency in vivo despite modest synergy in vitro .

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.

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