scholarly journals Divergent Effect of Cobalt and Beryllium Salts on the Fate of Peripheral Blood Monocytes and T Lymphocytes

2010 ◽  
Vol 119 (2) ◽  
pp. 257-269 ◽  
Author(s):  
F. Paladini ◽  
E. Cocco ◽  
I. Potolicchio ◽  
H. Fazekasova ◽  
G. Lombardi ◽  
...  
2016 ◽  
Vol 12 (1) ◽  
Author(s):  
Rohana P. Dassanayake ◽  
Sally A. Madsen-Bouterse ◽  
Thomas C. Truscott ◽  
Dongyue Zhuang ◽  
Michelle R. Mousel ◽  
...  

1997 ◽  
Vol 272 (5) ◽  
pp. L1025-L1029 ◽  
Author(s):  
M. J. Coffey ◽  
C. Woffendin ◽  
S. M. Phare ◽  
R. M. Strieter ◽  
D. M. Markovitz

Infection with human immunodeficiency virus (HIV)-1 most often leads to the development of acquired immune deficiency syndrome, which may manifest with opportunistic infections, many of which occur in the lung. Mononuclear phagocytes infected by HIV-1, being relatively resistant to its cytopathic effects, potentially act as a reservoir for the virus. The alveolar macrophage (AM), a differentiated lung tissue macrophage, is readily infected by HIV-1, after which the virus becomes relatively dormant. C-C chemokines, secreted by CD8 T lymphocytes and other cells, are known to suppress HIV replication in lymphocytes. In view of this observation, and the relative increase in CD8+ T lymphocytes during HIV-1 disease, particularly in the lung, we hypothesized that C-C chemokines might play a key role in suppressing HIV-1 replication in AM. We examined the effect of the C-C chemokines macrophage inflammatory protein (MIP)-1 alpha, MIP-1 beta, and regulated on activation normal T cell expressed and secreted (RANTES) singly and in combination on HIV-1 replication in peripheral blood monocytes (PBM) and AM infected in vitro. Our findings indicate that RANTES suppresses HIV-1 replication, as measured by reverse transcriptase activity, in PBM (41.3 +/- 15.2% of control, n = 3, P < 0.05) and AM (30.3 +/- 7.8% of control, n = 3, P < 0.05) in a dose-dependent manner. The other C-C chemokines had no significant effect singly (MIP-1 alpha PBM: 64.8 +/- 21.9%; AM: 115.0 +/- 2.4% of control; MIP-1 beta PBM: 68 +/- 19.6; AM: 63.3 +/- 26.2% of control) but modestly decreased HIV replication when incubated in addition to RANTES (24.5 +/- 6.5% of control). These observations suggest that RANTES plays a key role in modulating HIV-1 replication in mononuclear phagocytes in the blood and lung, and this may have therapeutic implications for prevention and/or treatment of HIV disease.


1997 ◽  
Vol 55 (2) ◽  
pp. 109-113 ◽  
Author(s):  
Angelos Koutsonikolis ◽  
Soichi Haraguchi ◽  
Emerita N. Brigino ◽  
Una E. Owens ◽  
Robert A. Good ◽  
...  

1996 ◽  
Vol 81 (2) ◽  
pp. 794-800 ◽  
Author(s):  
W. M. Foster ◽  
M. Wills-Karp ◽  
C. G. Tankersley ◽  
X. Chen ◽  
N. C. Paquette

Intermittent exposure of the human lung to ambient levels of ozone (O3) was assayed in systemic fluids by using serum alpha-tocopherol (ST) as a gauge of oxidative stress and the blastogenic activity of peripheral blood monocytes as an index of immune function. Healthy men (n = 10) were evaluated over 3 consecutive days (130 min/day) of chamber exposure to O3 and filtered air (FA); subjects alternated between rest and light treadmill exercise during exposures. For O3, the level was varied at 20-min intervals, i.e., 250, 350, 450, 450, 350, and 250 parts/billion, and concluded with 10 min at 250 parts/billion. ST was quantitated by high-performance liquid chromatography techniques, and T-lymphocyte blastogenesis was measured in cell cultures of peripheral blood monocytes by comparing [3H]thymidine incorporation in mitogen-stimulated (concanavalin A) and nonstimulated cells. After the third day of O3 at 20 h postexposure, ST levels were reduced significantly compared with the FA control subjects (down 14%; -0.96 mumol/l). Mitogen-activated T lymphocytes exhibited a 61% increase in blastogenic activity after 3 days of O3 exposure, significant compared with the proliferative activity of activated T lymphocytes collected after FA or before O3. Acute airway function was impaired by O3, e.g., on day 1, the forced vital capacity and forced expiratory volume in 1 s were decreased 8% (-0.92 liter) and 14% (-0.86 l/s), respectively, from preexposure values, and full recovery was delayed beyond 24 h. Effects of O3 exposure on cellular and biochemical markers increased in magnitude after each exposure and did not parallel the apparent adaptability of bronchial sensitivity to O3.


1982 ◽  
Vol 63 (5) ◽  
pp. 41-42
Author(s):  
S. S. Lebenzon ◽  
D. N. Mayansky ◽  
E. A. Spiridonova ◽  
A. V. Vasyunin ◽  
I. V. Altukhova ◽  
...  

The indices of humoral and cellular immunity were studied in 10 patients with typical and 7 atypical (carriage) forms of diphtheria infection. The highest level of antibodies (4.25 1.2 AU / ml) was in carriers of diphtheria bacteria, and the lowest (0.07 AU / ml) was in patients with toxic diphtheria. Disturbances in the structure of cellular immunogomeostasis - a decrease in the total number of T-lymphocytes, an increase in Ta-ROK, an increase in the functional activity of phagocytic neutrophils and peripheral blood monocytes - were found in all and were most pronounced in patients with toxic diphtheria. In children, according to epidemiological indications, vaccinated with ADS, while the number of T-lymphocytes was preserved, all other studied parameters turned out to be increased.


2004 ◽  
Vol 287 (2) ◽  
pp. L332-L343 ◽  
Author(s):  
Rachael Barber ◽  
George S. Baillie ◽  
Reinhard Bergmann ◽  
Malcolm C. Shepherd ◽  
Ruth Sepper ◽  
...  

The expression profile of a panel of 15 cAMP phosphodiesterase isoforms was determined for inflammatory cell types of relevance to chronic obstructive pulmonary disease (COPD). In particular, the expression profiles for bronchoalveolar macrophages, peripheral blood monocytes, T lymphocytes, and neutrophils from smokers with and without COPD were compared. The phosphodiesterase expression profile was also analyzed for peripheral blood monocytes, T lymphocytes, and neutrophils from nonsmokers and compared with smokers. Qualitative RT-PCR identified transcripts for PDE4A10, PDE4A7, PDE4B1, PDE4B2, PDE4D1, and PDE4D2 isoforms as well as transcripts for both PDE3B and PDE7A in T cells, monocytes, and macrophages in all subjects. Transcripts for PDE4B3 and PDE4D4 were not observed in any of the cell types investigated. PDE4C was detected in all cells analyzed except for T cells. The long PDE4A4, PDE4D3, and PDE4D5 isoforms exhibited cell type-specific expression patterns. Semiquantitative and real-time quantitative RT-PCR were used to analyze differential expression between disease states and between cell types. PDE4A4 was found significantly upregulated in lung macrophages from smokers with COPD when compared with control smokers. Furthermore, PDE4A4 as well as PDE4B2 transcripts were detected in higher amounts in peripheral blood monocytes of smokers when compared with nonsmokers. Finally, PDE4D5 and PDE4C were differentially regulated in lung macrophages when compared with monocytes of the same subjects, irrespective of the disease state. The data obtained suggest that PDE4A4 may be relevant as a macrophage-specific anti-inflammatory target for COPD.


1993 ◽  
Vol 70 (02) ◽  
pp. 273-280 ◽  
Author(s):  
Janos Kappelmayer ◽  
Satya P Kunapuli ◽  
Edward G Wyshock ◽  
Robert W Colman

SummaryWe demonstrate that in addition to possessing binding sites for intact factor V (FV), unstimulated peripheral blood monocytes also express activated factor V (FVa) on their surfaces. FVa was identified on the monocyte surface by monoclonal antibody B38 recognizing FVa light chain and by human oligoclonal antibodies H1 (to FVa light chain) and H2 (to FVa heavy chain) using immunofluorescence microscopy and flow cytometry. On Western blots, partially cleaved FV could be identified as a 220 kDa band in lysates of monocytes. In addition to surface expression of FVa, monocytes also contain intracellular FV as detected only after permeabilization by Triton X-100 by monoclonal antibody B10 directed specifically to the Cl domain not present in FVa. We sought to determine whether the presence of FV in peripheral blood monocytes is a result of de novo synthesis.Using in situ hybridization, no FV mRNA could be detected in monocytes, while in parallel control studies, factor V mRNA was detectable in Hep G2 cells and CD18 mRNA in monocytes. In addition, using reverse transcriptase and the polymerase chain reaction, no FV mRNA was detected in mononuclear cells or in U937 cells, but mRNA for factor V was present in Hep G2 cells using the same techniques. These data suggest that FV is present in human monocytes, presumably acquired by binding of plasma FV, and that the presence of this critical coagulation factor is not due to de novo synthesis.


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