Displacement of alveolar macrophages in air space of human lung

1995 ◽  
Vol 33 (4) ◽  
pp. 575-581 ◽  
Author(s):  
L. Gradoń ◽  
A. Podgórski
Keyword(s):  
Alveolar Macrophages ◽  
Human Lung ◽  
Air Space

scholarly journals Characterization of Early Stages of Human Alveolar Infection by the Q Fever AgentCoxiella burnetii

2019 ◽  
Vol 87 (5) ◽  
Author(s):  
Amanda L. Dragan ◽  
Richard C. Kurten ◽  
Daniel E. Voth
Keyword(s):  
Epithelial Cells ◽  
Lung Tissue ◽  
Alveolar Macrophages ◽  
Human Lung ◽  
Q Fever ◽  
Cell Types ◽  
Alveolar Epithelial Cells ◽  
Human Lung Tissue ◽  
Content Type ◽  
Alveolar Epithelial

ABSTRACTHuman Q fever is caused by the intracellular bacterial pathogenCoxiella burnetii. Q fever presents with acute flu-like and pulmonary symptoms or can progress to chronic, severe endocarditis. After human inhalation,C. burnetiiis engulfed by alveolar macrophages and transits through the phagolysosomal maturation pathway, resisting the acidic pH of lysosomes to form a parasitophorous vacuole (PV) in which to replicate. Previous studies showed thatC. burnetiireplicates efficiently in primary human alveolar macrophages (hAMs) inex vivohuman lung tissue. AlthoughC. burnetiireplicates in most cell typesin vitro, the pathogen does not grow in non-hAM cells of human lung tissue. In this study, we investigated the interaction betweenC. burnetiiand other pulmonary cell types apart from the lung environment.C. burnetiiformed a prototypical PV and replicated efficiently in human pulmonary fibroblasts and in airway, but not alveolar, epithelial cells. Atypical PV expansion in alveolar epithelial cells was attributed in part to defective recruitment of autophagy-related proteins. Further assessment of theC. burnetiigrowth niche showed that macrophages mounted a robust interleukin 8 (IL-8), neutrophil-attracting response toC. burnetiiand ultimately shifted to an M2-polarized phenotype characteristic of anti-inflammatory macrophages. Considering our findings together, this study provides further clarity on the uniqueC. burnetii-lung dynamic during early stages of human acute Q fever.

Asbestos Stimulates Alveolar Macrophages to Release a Factor Causing Human Lung Fibroblasts to Replicate

CHEST Journal ◽  
1981 ◽  
Vol 80 (1) ◽  
pp. 38S-39S ◽  
Author(s):  
P. Bitterman ◽  
S. Rennard ◽  
C. Schoenberger ◽  
Ronald Crystal
Keyword(s):  
Alveolar Macrophages ◽  
Human Lung ◽  
Lung Fibroblasts ◽  
Human Lung Fibroblasts

scholarly journals Ultrastructural immunogold localization of prostaglandin endoperoxide synthase (cyclooxygenase) to non-membrane-bound cytoplasmic lipid bodies in human lung mast cells, alveolar macrophages, type II pneumocytes, and neutrophils.

1992 ◽  
Vol 40 (6) ◽  
pp. 759-769 ◽  
Author(s):  
A M Dvorak ◽  
E Morgan ◽  
R P Schleimer ◽  
S W Ryeom ◽  
L M Lichtenstein ◽  
...  
Keyword(s):  
Mast Cells ◽  
Alveolar Macrophages ◽  
Human Lung ◽  
Cell Types ◽  
Type Ii ◽  
Lipid Bodies ◽  
Prostaglandin Endoperoxide ◽  
Isolated Lung ◽  
Membrane Bound ◽  
Eicosanoid Formation

Lipid bodies are non-membrane-bound, lipid-rich cytoplasmic inclusions that occur in many mammalian cell types. Because lipid bodies are more prominent in cells associated with inflammation and are repositories of arachidonyl-phospholipids, a role for lipid bodies in the oxidative metabolism of arachidonic acid to form eicosanoids has been suggested. To evaluate further whether lipid bodies, in addition to serving as non-membranous sources of substrate arachidonate, are involved in eicosanoid formation, we used cells isolated from human lung to investigate the intracellular localization of prostaglandin endoperoxide (PGH) synthase (cyclooxygenase), the key initial, rate-limiting enzyme in the formation of prostaglandins and thromboxanes. Isolated lung cells containing a mixture of mast cells, alveolar macrophages, Type II alveolar pneumocytes, and neutrophils from short-term cultures were fixed in suspension in a dilute aldehyde mixture, post-fixed in osmium tetroxide, stained en bloc with uranyl acetate, dehydrated in a graded series of alcohols, and embedded in Epon. A post-embedding immunogold procedure was used with a primary PGH synthase monoclonal antibody and 20-nm gold-conjugated secondary antibody to demonstrate enzyme locations. Specificity controls were also done. We found PGH synthase in lipid bodies of human lung mast cells, alveolar macrophages, Type II alveolar pneumocytes, and neutrophils. Specific secretory and lysosomal granules and plasma membranes did not express PGH synthase. Specificity controls, including omission of the primary antibody or substitution with an irrelevant antibody, were negative. Absorption of the specific PGH synthase antibody with purified solid-phase PGH synthase resulted in a marked reduction of label in lipid bodies of all four cell types. These findings establish the presence of PGH synthase in lipid bodies of human lung mast cells, alveolar macrophages, Type II alveolar pneumocytes, and neutrophils and, in concert with previous studies, suggest that these cytoplasmic lipid-rich organelles may be non-membrane sites of eicosanoid formation.

Endotoxin-stimulated alveolar macrophages impair lung epithelial Na+ transport by an L-Arg-dependent mechanism

1994 ◽  
Vol 266 (5) ◽  
pp. C1330-C1341 ◽  
Author(s):  
C. G. Compeau ◽  
O. D. Rotstein ◽  
H. Tohda ◽  
Y. Marunaka ◽  
B. Rafii ◽  
...  
Keyword(s):  
Ion Transport ◽  
Alveolar Macrophages ◽  
Single Channel ◽  
Short Circuit ◽  
Na Transport ◽  
Epithelial Ion Transport ◽  
Lung Epithelial ◽  
Air Space ◽  
Distal Lung ◽  
Dependent Mechanism

The Na+ transport function of alveolar epithelium represents an important mechanism for air space fluid clearance after acute lung injury. We studied the effect of endotoxin-stimulated rat alveolar macrophages on lung epithelial ion transport and permeability in vitro. Cultured rat distal lung (alveolar) epithelial monolayers incubated with both endotoxin and macrophages demonstrated a 75% decline in transepithelial resistance and a selective 60% reduction in amiloride-sensitive short-circuit current (Isc). Single-channel patch-clamp analysis demonstrated a 60% decrease in the density of 25-pS nonselective cation (NSC) channels on the apical membrane of epithelium exposed to both endotoxin and macrophages. A concurrent reduction in epithelial F-actin content suggested a role for actin depolymerization in mediating this effect. Incubation of cocultures with the methylated L-arginine (Arg) derivative NG-monomethyl-L-arginine prevented the reduction in epithelial Isc, as did substitution of L-Arg with D-Arg or incubation in L-Arg-free medium. Furthermore, the stable and products of Arg metabolism were found to have no effect on epithelial ion transport. These studies show that endotoxin-stimulated alveolar macrophages impair distal lung epithelial ion transport by an L-Arg-dependent mechanism by inactivating amiloride-sensitive 25-pS NSC channels. This may represent a novel mechanism whereby local inflammatory cells regulate lung epithelial ion transport. This could affect the ability of the lung to clear fluid from the air space.

scholarly journals Physiological and biochemical markers of alveolar epithelial barrier dysfunction in perfused human lungs

2007 ◽  
Vol 293 (1) ◽  
pp. L52-L59 ◽  
Author(s):  
James A. Frank ◽  
Raphael Briot ◽  
Jae Woo Lee ◽  
Akitoshi Ishizaka ◽  
Tokujiro Uchida ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
Fluid Balance ◽  
Human Lung ◽  
Biological Marker ◽  
Epithelial Injury ◽  
Alveolar Epithelial ◽  
Lung Fluid ◽  
Lung Fluid Balance ◽  
Human Lungs ◽  
Air Space

To study air space fluid clearance (AFC) under conditions that resemble the clinical setting of pulmonary edema in patients, we developed a new perfused human lung preparation. We measured AFC in 20 human lungs rejected for transplantation and determined the contribution of AFC to lung fluid balance. AFC was then compared with air space and perfusate levels of a biological marker of epithelial injury. The majority of human lungs rejected for transplant had intact basal (75%) and β2-adrenergic agonist-stimulated (70%) AFC. For lungs with both basal and stimulated AFC, the basal AFC rate was 19 ± 10%/h, and the β2-adrenergic-stimulated AFC rate was 43 ± 13%/h. Higher rates of AFC were associated with less lung weight gain (Pearson coefficient −0.90, P < 0.0001). Air space and perfusate levels of the type I pneumocyte marker receptor for advanced glycation end products (RAGE) were threefold and sixfold higher, respectively, in lungs without basal AFC compared with lungs with AFC ( P < 0.05). These data show that preserved AFC is a critical determinant of favorable lung fluid balance in the perfused human lung, raising the possibility that β2-agonist therapy to increase edema fluid clearance may be of value for patients with acute lung injury and pulmonary edema. Also, although additional studies are needed, a biological marker of alveolar epithelial injury may be useful clinically in predicting preserved AFC.

Biological Effects of Mount Saint Helens Volcanic Ash on Cultured Human Alveolar Macrophages

1984 ◽  
Vol 3 (1) ◽  
pp. 25-35 ◽  
Author(s):  
T. L. McLemore ◽  
J. E. Mauldin ◽  
M. V. Marshall ◽  
R. Teague ◽  
G. Ford ◽  
...  
Keyword(s):  
Cell Viability ◽  
Amorphous Silica ◽  
Alveolar Macrophages ◽  
Volcanic Ash ◽  
Human Lung ◽  
Lung Cells ◽  
Chrysotile Asbestos ◽  
Cytotoxic Effects ◽  
Airborne Particulates ◽  
Human Lung Cells

Free alveolar macrophages (FAMs) obtained by bronchoalveolar lavage from healthy nonsmoking volunteers were incubated with varying concentrations (0–300 μg/ml) of Mt. Saint Helens volcanic ash obtained from either Portland, Oregon, or Pullman, Washington, to assess the cytotoxic effects of the ash on human lung cells. Trypan dye exclusion techniques were employed for assessment of cell viability. Following the initial 24 hour culture with the Portland ash samples, decreased viability was observed at all ash concentrations (P < 0.001 in all instances), and further decreases in viability were noted at 48 and 72 hours for all concentrations of ash tested (P < 0.001 in all instances). When the Pullman, Washington, ash sample was evaluated, a decrease in cell viability was noted for the 300 μg/ml concentration (P < 0.017) after the initial 24 hours in culture. Further decreases in cell viability were noted only when cells were cultured for longer time intervals (48 and 72 hours) (P < 0.05 in all instances). Differences in cellular response to the 2 ash samples were further investigated by exposing FAMs from a single individual to the 2 different types of ash. These studies demonstrated similar cytotoxic effects of the 2 ash samples at all concentrations and times tested (P < 0.30 in all instances) with the exception of the 100 μg/ml concentrations at 72 hours (P < 0.020). These data suggest that the differences observed between the 2 types of ash in the independent studies are probably related to interindividual variation in FAM response to the ash rather than to differences in the cytotoxicities of the 2 ash samples. Cytotoxicity of the volcanic ash was also compared with other environmentally relevant airborne particulates, such as amosite and chrysotile asbestos, as well as amorphous and crystalline silica. These results demonstrated an intermediate cytotoxic effect of the ash between innocuous amorphous silica and the very cytotoxic chrysotile asbestos. The affinity for volcanic ash to adsorb tritiated benzo(a)pyrene (3H-BaP) was also compared with that of amorphous silica and amosite asbestos. These studies demonstrate that volcanic ash has intermediate adsorption qualities (4.3 ± 0.1; pmoles 3H-BaP adsorbed/μg particulate ± SD) between those of amorphous silica (1.9 ± 1.0) and amosite asbestos (7.8 ± 1.2) (P < 0.05 in all instances). These data suggest volcanic ash exhibits moderate biological properties compared with those of other environmentally important airborne particulates. Whether in vitro studies reflect in vivo response of human lung cells to the ash cannot be determined at this time, and follow-up of assessment of individuals exposed to the ash will be required to assess its long-term effects on pulmonary tissue.

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