Role of alveolar macrophage chemotaxis and phagocytosis in pulmonary clearance responses to inhaled particles: Comparisons among rodent species

1993 ◽  
Vol 26 (5) ◽  
pp. 412-422 ◽  
Author(s):  
David B. Warheit ◽  
Mark A. Hartsky
Keyword(s):  
Alveolar Macrophage ◽  
Rodent Species ◽  
Inhaled Particles ◽  
Pulmonary Clearance ◽  
Macrophage Chemotaxis

An integrated screening method for evaluating the pulmonary toxicity of inhaled particulates: Role of microscopic techniques in assessing pulmonary macrophage clearance functions

1990 ◽  
Vol 48 (3) ◽  
pp. 826-827
Author(s):  
David B. Warheit ◽  
Lena Achinko ◽  
Mark A. Hartsky
Keyword(s):  
Bronchoalveolar Lavage ◽  
Pulmonary Toxicity ◽  
Screening Method ◽  
Pulmonary Response ◽  
Inhaled Particles ◽  
Cytochemical Analysis ◽  
Pulmonary Macrophages ◽  
Integrated Screening

There is a great need for the development of a rapid and reliable bioassay to evaluate the pulmonary toxicity of inhaled particles. A number of methods have been proposed, including lung clearance studies, bronchoalveolar lavage analysis, and in vitro cytotoxicity tests. These methods are often limited in scope inasmuch as they measure only one dimension of the pulmonary response to inhaled, instilled or incubated dusts. Accordingly, a comprehensive approach to lung toxicity studies has been developed.To validate the method, rats were exposed for 6 hours or 3 days to various concentrations of either aerosolized alpha quartz silica (Si) or carbonyl iron (CI) particles. Cells and fluids from groups of sham and dust-exposed animals were recovered by bronchoalveolar lavage (BAL). Alkaline phosphatase, LDH and protein values were measured in BAL fluids at several time points postexposure. Cells were counted and evaluated for viability, as well as differential and cytochemical analysis. In addition, pulmonary macrophages (PM) were cultured and studied for morphology, chemotaxis, and phagocytosis by scanning electron microscopy.

scholarly journals Role of zinc insufficiency in fetal alveolar macrophage dysfunction and RSV exacerbation associated with fetal ethanol exposure

Alcohol ◽  
2019 ◽  
Vol 80 ◽  
pp. 5-16 ◽  
Author(s):  
Juna Konomi Johnson ◽  
Frank L. Harris ◽  
Xiao-Du Ping ◽  
Theresa W. Gauthier ◽  
Lou Ann S. Brown
Keyword(s):  
Alveolar Macrophage ◽  
Ethanol Exposure ◽  
Macrophage Dysfunction ◽  
Fetal Ethanol

Role of PGE2 Produced by Neoplastic Cells as Modulators of Macrophage Chemotaxis

1984 ◽  
pp. 223-233
Author(s):  
G. M. Pontieri ◽  
L. Lenti ◽  
M. Lipari ◽  
D. Lombardi ◽  
A. Zicari ◽  
...  
Keyword(s):  
Neoplastic Cells ◽  
Macrophage Chemotaxis

scholarly journals Seasonal variations in the oxidative stress and inflammatory potential of PM2.5 in Tehran using an alveolar macrophage model; The role of chemical composition and sources

2019 ◽  
Vol 123 ◽  
pp. 417-427 ◽  
Author(s):  
Ahlam H. Al Hanai ◽  
Dagmara S. Antkiewicz ◽  
Jocelyn D.C. Hemming ◽  
Martin M. Shafer ◽  
Alexandra M. Lai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chemical Composition ◽  
Alveolar Macrophage ◽  
Seasonal Variations

Immunomodulatory Role of PPAR-γ in Alveolar Macrophages

2008 ◽  
Vol 56 (2) ◽  
pp. 522-527 ◽  
Author(s):  
Raju C. Reddy
Keyword(s):  
Fatty Acids ◽  
Alveolar Macrophage ◽  
Alveolar Macrophages ◽  
Adaptive Immune System ◽  
Pulmonary Sarcoidosis ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Inhaled Particles ◽  
Ppar Γ ◽  
Inflammatory Stimuli

The lung is constantly exposed to inhaled pathogens and toxins yet totally dependent on the integrity of a delicate alveolar-capillary interface for its function. Much of the balance between protection and collateral damage rests on the alveolar macrophage, which not only phagocytoses inhaled particles but also modulates the activity of both innate and acquired immune systems to limit unnecessary or exuberant inflammation. In its resting state, the alveolar macrophage secretes anti-inflammatory mediators while limiting antigen presentation to the adaptive immune system. The alveolar macrophage's state of activation is regulated by a variety of factors, including the activity of the nuclear receptor peroxisome proliferator-activated receptor γ (PPAR-γ). Peroxisome proliferator-activated receptor γ agonists reduce the ability of inflammatory stimuli to activate the alveolar macrophage while simultaneously stimulating phagocytosis of both opsonized and unopsonized particles, via the Fcγ and CD36 receptors, respectively. All known endogenous PPAR-γ ligands are fatty acid derivatives, and macrophage-specific knockout of the enzyme that converts esterified fatty acids to free fatty acids results in severe lung inflammation. Peroxisome proliferator-activated receptor γ expression is reduced in alveolar macrophages from patients with pulmonary sarcoidosis and alveolar proteinosis, suggesting that the deficiency may play a role in pathogenesis of these diseases. In summary, these observations point to PPAR-γ in the context of the alveolar macrophage as a crucial factor in limiting excessive and possibly injurious inflammation in the lung.

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