Induction of microbial variants of Pseudomonas pseudomallei in cultured rabbit alveolar macrophages

1975 ◽  
Vol 21 (12) ◽  
pp. 2112-2115 ◽  
Author(s):  
Richard A. Kishimoto ◽  
Warren C. Eveland
Keyword(s):  
Alveolar Macrophages ◽  
Peritoneal Macrophages ◽  
Pseudomonas Pseudomallei

Cultured alveolar and peritoneal macrophages obtained from normal and immunized rabbits were used to induce wall-defective microbial variants of Pseudomonas pseudomallei. Variants were induced only by normal alveolar macrophages. The variants reverted to typical Pseudomonas forms either spontaneously or upon transfer into broth or agar.

In situ activation of mouse alveolar macrophages by aerosolized liposomal IFN-gamma and muramyl tripeptide

1996 ◽  
Vol 270 (3) ◽  
pp. L429-L434 ◽  
Author(s):  
P. Goldbach ◽  
S. Dumont ◽  
R. Kessler ◽  
P. Poindron ◽  
A. Stamm
Keyword(s):  
Alveolar Macrophages ◽  
Peritoneal Macrophages ◽  
Target Cells ◽  
Tumoricidal Activity ◽  
Ifn Gamma ◽  
In Situ Activation ◽  
Organ Specific ◽  
Thawing Procedure

Interferon-gamma (IFN-gamma) was entrapped with an efficiency of 30-40% in muramyl tripeptide-containing liposomes by a freeze-thawing procedure. A microcytotoxicity assay was developed to measure the tumoricidal activity of mouse alveolar macrophages (AM) against tumoral target cells with a colorimetric viability test. Free IFN-gamma and liposomal muramyl tripeptide phosphatidylethanolamine (MTP-PE) were found to be only slightly effective to activate in vitro AM, whereas encapsulation of both INF-gamma and MTP-PE within the same liposomes produced higher activation of AM. Aerosolized IFN-gamma and liposomal immunomodulators enhanced antitumor properties of AM recovered in mice 24 h postinhalation. Whereas free IFN-gamma also induced a substantial activation of peritoneal macrophages, liposomal encapsulation significantly reduced the systemic activity of inhaled immunomodulators. This approach provides a useful model for the compartmentalized organ-specific activation of AM in mice.

scholarly journals Lack of IL-10 synthesis by murine alveolar macrophages upon lipopolysaccharide exposure. Comparison with peritoneal macrophages

2000 ◽  
Vol 67 (4) ◽  
pp. 545-552 ◽  
Author(s):  
Laurent Salez ◽  
Monique Singer ◽  
Viviane Balloy ◽  
Christophe Créminon ◽  
Michel Chignard
Keyword(s):  
Alveolar Macrophages ◽  
Peritoneal Macrophages

scholarly journals Stimulatory Effects of Peroxisome Proliferator-Activated Receptor-γon FcγReceptor-Mediated Phagocytosis by Alveolar Macrophages

PPAR Research ◽  
2007 ◽  
Vol 2007 ◽  
pp. 1-8 ◽  
Author(s):  
David M. Aronoff ◽  
Carlos H. Serezani ◽  
Jennifer K. Carstens ◽  
Teresa Marshall ◽  
Srinivasa R. Gangireddy ◽  
...  
Keyword(s):  
Alveolar Macrophages ◽  
Peritoneal Macrophages ◽  
Receptor Expression ◽  
Cell Surface Receptor ◽  
Peroxisome Proliferator ◽  
Quiescent State ◽  
Peroxisome Proliferator Activated Receptor ◽  
Downstream Signaling ◽  
Surface Receptor ◽  
And Function

Alveolar macrophages abundantly express PPAR-γ, with both natural and synthetic agonists maintaining the cell in a quiescent state hyporesponsive to antigen stimulation. Conversely, agonists upregulate expression and function of the cell-surface receptor CD36, which mediates phagocytosis of lipids, apoptotic neutrophils, and other unopsonized materials. These effects led us to investigate the actions of PPAR-γagonists on the Fcγreceptor, which mediates phagocytosis of particles opsonized by binding of immunoglobulin G antibodies. We found that troglitazone, rosiglitazone, and 15-deoxy-Δ12,14-prostaglandinJ2increase the ability of alveolar, but not peritoneal, macrophages to carry out phagocytosis mediated by the Fcγreceptor. Receptor expression was not altered but activation of the downstream signaling proteins Syk, ERK-1, and ERK-2 was observed. Although it was previously known that PPAR-γligands stimulate phagocytosis of unopsonized materials, this is the first demonstration that they stimulate phagocytosis of opsonized materials as well.

scholarly journals Fungicidal activity of rabbit alveolar and peritoneal macrophages against Candida albicans

1980 ◽  
Vol 28 (3) ◽  
pp. 1001-1008
Author(s):  
R I Lehrer ◽  
L G Ferrari ◽  
J Patterson-Delafield ◽  
T Sorrell
Keyword(s):  
Candida Albicans ◽  
Alveolar Macrophages ◽  
Fungicidal Activity ◽  
Peritoneal Macrophages ◽  
Human Monocytes ◽  
Blood Monocytes ◽  
Human Granulocytes ◽  
The Mean ◽  
Macrophage Populations

We tested the ability of rabbit macrophages to kill Candida albicans in vitro. Resident (unstimulated) alveolar macrophages killed 28.1 +/- 1.9% of ingested organisms in 4 h, whereas resident peritoneal macrophages killed only 15.2 +/- 1.3% (mean +/- standard error of the mean, P < 0.01). Peritoneal macrophages obtained from rabbits treated 3 weeks earlier with complete Freund adjuvant showed enhanced candidacidal activity relative to normally resident peritoneal cells (28.2 +/- 3.1%, P < 0.01). Candidacidal activity by alveolar macrophages recovered from such treated animals was slightly enhanced relative to untreated alveolar macrophages (32.9 +/- 2.3%). Candidacidal activity by peritoneal and alveolar macrophages was not decreased by several agents (cyanide, azide, sulfadiazine, and phenylbutazone) that inhibit the ability of human blood monocytes to kill C. albicans. In contrast, candidacidal activity by alveolar macrophages was greatly diminished by iodoacetate, an ineffective inhibitor of this function in human monocytes. We conclude that rabbit macrophages kill C. albicans by a fungicidal mechanism distinct from the peroxidase-H2O2 mechanism of human granulocytes and monocytes, and that the fungicidal properties of peritoneal and alveolar macrophage populations are enhanced after nonspecific stimulation with complete Freund adjuvant.

scholarly journals The Effects of Particulate Matter on C57BL/6 Peritoneal and Alveolar Macrophages

2020 ◽  
Author(s):  
Hoda Rahmani ◽  
Somaye Sadeghi ◽  
Niloofar Taghipour ◽  
Mohsen Roshani ◽  
Davar Amani ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Alveolar Macrophages ◽  
Critical Role ◽  
Peritoneal Macrophages ◽  
Considerable Effect ◽  
Epidemiologic Studies ◽  
Phagocytic Capacity ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Inflammatory Phenotype

The presence of ambient particulate matter (PM) poses more dangers to human health than that of other common air pollutants such as Carbon dioxide (Co2) and ozone.  Epidemiologic studies show a direct correlation between PM and the risk of respiratory and cardiovascular diseases. The immune system seems to play a critical role in the process of these diseases. The main goal of this study was to investigate the effect of Tehran particulate matter in two aerodynamic diameters (PM2.5 and PM10) on alveolar macrophages (AM) from C57/BL6 mice. To evaluate the inflammatory effects of PMs, cultured alveolar, and peritoneal macrophages were treated with PM2.5 & PM10 (concentrations of 5 µg/mL and 10 µg/mL). Tumor necrosis factor-alpha (TNF-α) and IL-10 (representatives of inflammatory and anti-inflammatory cytokines, respectively) were assessed in the culture supernatant by ELISA. Expression of arginase and inducible nitric oxide synthase (iNOS) genes was carried out by quantitative real-time PCR. Different functional types of cultured alveolar macrophages (M1, M2) were also determined in this study. Our results suggest that PM2.5 induces M1 inflammatory phenotype in comparison with PM10. We found Also, an increase in TNF-α and M1-related gene expression (iNOS), as well as a decrease in both IL-10 and M2 phenotype genes (Arginase). Moreover, a reduction in phagocytic capacity and increased apoptosis function of macrophage cells were detected. PM2.5 as a major component in hydrocarbons has a considerable effect on polarizing the alveolar macrophages to an inflammatory phenotype and eliciting lung inflammation in mice.

scholarly journals Glucose Stimulates Phagocytosis of UnopsonizedPseudomonas aeruginosa by Cultivated Human Alveolar Macrophages

1999 ◽  
Vol 67 (1) ◽  
pp. 16-21 ◽  
Author(s):  
Simon Y. C. Wong ◽  
Lila M. Guerdoud ◽  
André Cantin ◽  
David P. Speert
Keyword(s):  
Glucose Transport ◽  
Alveolar Macrophages ◽  
Peritoneal Macrophages ◽  
In Vitro Cultivation ◽  
Transport Activity ◽  
Glucose Effect ◽  
Effect Of Glucose ◽  
Level 2 ◽  
Phagocytic Response

ABSTRACT Glucose has previously been shown to increase the in vitro phagocytosis of unopsonized Pseudomonas aeruginosa by freshly explanted murine peritoneal macrophages (PM) and cultivated alveolar macrophages (AM). This study examined the effect of glucose on the same phagocytosis process in human AM in order to determine whether this phenomenon is conserved among species. Freshly explanted human AM phagocytosed unopsonized P. aeruginosa at a low level (2 bacteria/macrophage/30 min), whereas mouse AM ingested a negligible number of P. aeruginosa (0.01 bacterium/macrophage/30 min). Glucose had no effect on this or other phagocytic processes in freshly explanted mouse or human AM. However, following in vitro cultivation for 72 h, human AM phagocytosed three to four times more unopsonized P. aeruginosa than did freshly explanted cells, but only in the presence of glucose. This glucose-inducible phagocytic response had also been observed in cultivated murine AM. Although similar increases were also detected for the phagocytosis of latex particles and complement-coated sheep erythrocytes by cultivated human AM, these processes were not glucose dependent. The lack of response to glucose in freshly explanted mouse AM was attributed to insufficient glucose transport; however, freshly explanted human AM exhibited significant facilitative glucose transport activity that was inhibitable by cytochalasin B and phloretin. Taken together, these results suggest that the process of glucose-inducible phagocytosis of unopsonized P. aeruginosa is conserved among macrophages from different species, including humans, and that AM, but not PM, required cultivation for this glucose effect to occur. Glucose transport by AM appears to be necessary but not sufficient for phagocytosis of unopsonized P. aeruginosa.

Basal activation of protein kinase C in rat alveolar macrophages: implications for arachidonate metabolism

1991 ◽  
Vol 261 (6) ◽  
pp. L462-L471 ◽  
Author(s):  
M. Peters-Golden ◽  
R. W. McNish ◽  
P. H. Sporn ◽  
K. Balazovich
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Alveolar Macrophages ◽  
Cell Types ◽  
Peritoneal Macrophages ◽  
Mononuclear Phagocyte ◽  
Ionophore A23187 ◽  
Lipoxygenase Pathway ◽  
Macrophage Function ◽  
Kinase C

Alveolar macrophages (AM) exhibit numerous functional differences from other mononuclear phagocyte populations, even though they are derived from a common circulating monocytic precursor. Yet no differences in fundamental signaling mechanisms uniquely expressed by AM have been elucidated to date. Protein kinase C (PKC) is one signal transduction mechanism thought to have an important role in regulating macrophage function and about which little information exists for AM. This study was undertaken to assess the state of activation of PKC in cultured resident rat AM compared with resident rat peritoneal macrophages (PM) and the means by which active PKC regulates arachidonic acid (AA) metabolism in the two cell types. As assessed by a histone phosphorylation assay, resting AM, in contrast to PM, exhibited constitutive activation of PKC as evidenced by localization of a majority of PKC activity to the membrane fraction. Ionophore A23187-stimulated release and metabolism of AA were attenuated by depletion of or inhibition of cellular PKC activity in AM but not in PM. In contrast, A23187-stimulated AA metabolism was augmented by activation of PKC to a greater extent in PM than in AM. Results from both cell types indicated that the 5-lipoxygenase pathway was particularly upregulated by PKC activation. We conclude that activation of PKC occurs uniquely during macrophage residence in the alveolar space and that this property as well as the downregulation of PKC which results have profound consequences for the regulation of at least one important macrophage function, the synthesis of bioactive eicosanoids.

Minocycline inhibits peritoneal macrophages but activates alveolar macrophages in acute pancreatitis

2015 ◽  
Vol 71 (4) ◽  
pp. 839-846 ◽  
Author(s):  
Laia Bonjoch ◽  
Sabrina Gea-Sorlí ◽  
Joaquin Jordan ◽  
Daniel Closa
Keyword(s):  
Acute Pancreatitis ◽  
Alveolar Macrophages ◽  
Peritoneal Macrophages

scholarly journals Elastase secretion by peritoneal exudative and alveolar macrophages.

1977 ◽  
Vol 146 (3) ◽  
pp. 802-808 ◽  
Author(s):  
R White ◽  
H S Lin ◽  
C Kuhn
Keyword(s):  
Alveolar Macrophages ◽  
Culture Medium ◽  
Peritoneal Macrophages ◽  
Ph Optimum ◽  
Elastolytic Activity ◽  
Additional Stimulation ◽  
Periodic Changes

Mouse alveolar macrophages (AM) cultured in the absence of serum secrete an elastolytic enzyme. The elastase from AM resembles the previously described elastase from peritoneal macrophages (PM) in pH optimum and inhibition profile. The macrophage enzymes do not appear to be stored, and with periodic changes in the culture medium, accumulate extracellularly for up to 10 days. Resident PM produce barely detectable levels of extracellular elastase unless given a phagocytic load. Thioglycollate-stimulated peritoneal exudative macrophages (PEM), however, secret easily detectable levels of elastase, which can be further increased with a phagocytic load. Without any additional stimulation, AM secret an elastolytic activity comparable to that of the PEM receiving a phagocytic load, but unlike PM they do not increase elastase secretion after phagocytosis.

Sign in / Sign up

Export Citation Format

Share Document