TIME-DEPENDENT APOPTOSIS OF ALVEOLAR MACROPHAGES FROM RATS EXPOSED TO BLEOMYCIN: INVOLVEMENT OF TNF RECEPTOR 2

2004 ◽  
Vol 67 (17) ◽  
pp. 1391-1406 ◽  
Author(s):  
H. W. Zhao ◽  
S. Y. Hu ◽  
M. W. Barger ◽  
J. K. H. Ma ◽  
V. Castranova ◽  
...  
Keyword(s):  
Alveolar Macrophages ◽  
Time Dependent ◽  
Tnf Receptor

Intraoperative Modulation of Alveolar Macrophage Function during Isoflurane and Propofol Anesthesia 

1998 ◽  
Vol 89 (5) ◽  
pp. 1125-1132 ◽  
Author(s):  
Naoki Kotani ◽  
Hiroshi Hashimoto ◽  
Daniel I. Sessler ◽  
Atsuhiro Kikuchi ◽  
Akiko Suzuki ◽  
...  
Keyword(s):  
Alveolar Macrophage ◽  
Alveolar Macrophages ◽  
Orthopedic Surgery ◽  
Pulmonary Infection ◽  
Time Dependent ◽  
Critical Part ◽  
Isoflurane Anesthesia ◽  
Immunologic Function ◽  
Over Time ◽  
Number Of Particles

Background Alveolar macrophages are a critical part of the defense against pulmonary infection. Thus the authors determined time-dependent changes in alveolar macrophage functions in patients having surgery who were anesthetized with isoflurane or propofol. Methods Patients anesthetized with propofol (n = 30) or isoflurane (n = 30) during orthopedic surgery were studied. Alveolar macrophages were harvested by bronchoalveolar lavage immediately, and 2, 4, and 6 h after induction anesthesia and at the end of surgery. The fraction of aggregated and nonviable macrophages was determined. Then phagocytosis was measured by ingestion of opsonized and unopsonized particles. Finally, microbicidal activity was determined as the ability of the macrophages to kill Listeria monocytogenes directly. Results Demographic and morphometric characteristics of the patients given propofol and isoflurane were similar, as were their levels of pulmonary function and hemodynamic responses. The fraction of alveolar macrophages ingesting opsonized and unopsonized particles, and the number of particles ingested, decreased significantly over time, with the decrease slightly but significantly greater during isoflurane anesthesia. Microbicidal function decreased progressively during anesthesia and surgery, with the decrease almost twice as great during isoflurane compared with propofol anesthesia. The fraction of aggregated macrophages and recovered neutrophils increased over time in the patients given each anesthetic. Conclusions Pulmonary immunologic function changed progressively during anesthesia and surgery. The data from this study suggest that pulmonary defenses are modulated by the type of anesthesia and by the duration of anesthesia and surgery.

scholarly journals THP-1 Cell Apoptosis in Response to Mycobacterial Infection

2003 ◽  
Vol 71 (1) ◽  
pp. 254-259 ◽  
Author(s):  
Carrie J. Riendeau ◽  
Hardy Kornfeld
Keyword(s):  
Alveolar Macrophages ◽  
Mycobacterial Infection ◽  
Host Cells ◽  
Tnf Receptor ◽  
Wild Type ◽  
Necrosis Factor Alpha ◽  
Retroviral Transduction ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT We previously reported that Mycobacterium tuberculosis infection primes human alveolar macrophages (HAM) for tumor necrosis factor alpha (TNF-α)-mediated apoptosis and that macrophage apoptosis is associated with killing internalized bacilli. Virulent mycobacterial strains elicit much less apoptosis than attenuated strains, implying that apoptosis is a defense against intracellular infection. The present study evaluated the potential for phorbol myristate acetate-differentiated THP-1 cells to mimic this response of primary macrophages. Consistent with the behavior of alveolar macrophages, attenuated M. tuberculosis H37Ra and Mycobacterium bovis BCG strongly induce THP-1 apoptosis, which requires endogenous TNF. THP-1 apoptosis is associated with reduced viability of infecting BCG. In contrast, virulent wild-type M. tuberculosis H37Rv and M. bovis do not increase THP-1 apoptosis over baseline. BCG induced early activation of caspase 10 and 9, followed by caspase 3. In contrast, wild-type M. bovis infection failed to activate any caspases in THP-1 cells. BCG-induced THP-1 apoptosis is blocked by retroviral transduction with vectors expressing crmA but not bcl-2. We conclude that differentiated THP-1 cells faithfully model the apoptosis response of HAM. Analysis of the THP-1 cell response to infection with virulent mycobacteria suggests that TNF death signals are blocked proximal to initiator caspase activation, at the level of TNF receptor 1 or its associated intracytoplasmic adaptor complex. Interference with TNF death signaling may be a virulence mechanism that allows M. tuberculosis to circumvent innate defenses leading to apoptosis of infected host cells.

scholarly journals Impairment of Endotoxin-Induced Macrophage Inflammatory Protein 2 Gene Expression in Alveolar Macrophages in Streptozotocin-Induced Diabetes in Mice

2000 ◽  
Vol 68 (5) ◽  
pp. 2925-2929 ◽  
Author(s):  
Hideaki Amano ◽  
Hidefumi Yamamoto ◽  
Masachika Senba ◽  
Kazunori Oishi ◽  
Shoichi Suzuki ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Alveolar Macrophages ◽  
Neutrophil Recruitment ◽  
Time Dependent ◽  
Diabetic Mice ◽  
Lps Challenge ◽  
Inflammatory Protein ◽  
Streptozotocin Induced Diabetes ◽  
Tract Infections ◽  
Macrophage Inflammatory Protein

ABSTRACT To elucidate the mechanism of the high incidence of lower respiratory tract infections in patients with diabetes mellitus, we investigated the kinetics of production of macrophage inflammatory protein 2 (MIP-2), an important mediator of lung neutrophil recruitment, using mice with streptozotocin-induced diabetes. Intratracheal challenge with 1 mg of lipopolysaccharide (LPS), an endotoxin, per kg of body weight resulted in a time-dependent increase in the levels of MIP-2 protein in bronchoalveolar lavage (BAL) fluid, with the peak concentration (49.4 ± 13 ng/ml) occurring at 3 h and significant neutrophil accumulation becoming apparent by 3 h in normal mice. In diabetic mice, the peak level of MIP-2 protein in BAL fluid did not occur until 6 h and was reduced to 21.9 ± 10 ng/ml. Immunohistochemical studies using anti-MIP-2 antibody confirmed that the main cellular source of MIP-2 in the lung after LPS challenge was alveolar macrophages (AMs) in normal mice. The lungs in diabetic mice, however, showed no AMs staining for MIP-2 within 3 h after LPS challenge. PCR analysis using whole-lung RNA showed a time-dependent increase in MIP-2 mRNA levels after LPS instillation. The level of MIP-2 mRNA in diabetic mice was markedly decreased compared to that in normal mice. Our results indicate that impairment of MIP-2 mRNA expression in the AMs in diabetic mice resulted in delayed neutrophil recruitment in the lungs, and this may explain the development and progression of pulmonary infection in diabetes mellitus.

Quantification of Silica Uptake by Alveolar Macrophages - An Emperical Scanning Electron Microprobe Method

1982 ◽  
Vol 40 ◽  
pp. 332-333
Author(s):  
V. V. Damiano ◽  
R. P. Daniele ◽  
H. T. Tucker ◽  
J. H. Dauber
Keyword(s):  
Quantitative Analysis ◽  
Alveolar Macrophages ◽  
Bulk Sample ◽  
Silica Particles ◽  
Empirical Method ◽  
Phagocytic Cells ◽  
Calibration Standards ◽  
X Ray ◽  
Accurate Quantitative Analysis ◽  
Scanning Electron

An important example of intracellular particles is encountered in silicosis where alveolar macrophages ingest inspired silica particles. The quantitation of the silica uptake by these cells may be a potentially useful method for monitoring silica exposure. Accurate quantitative analysis of ingested silica by phagocytic cells is difficult because the particles are frequently small, irregularly shaped and cannot be visualized within the cells. Semiquantitative methods which make use of particles of known size, shape and composition as calibration standards may be the most direct and simplest approach to undertake. The present paper describes an empirical method in which glass microspheres were used as a model to show how the ratio of the silicon Kα peak X-ray intensity from the microspheres to that of a bulk sample of the same composition correlated to the mass of the microsphere contained within the cell. Irregular shaped silica particles were also analyzed and a calibration curve was generated from these data.

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