scholarly journals Phagocytosis of senescent neutrophils by human monocyte-derived macrophages and rabbit inflammatory macrophages.

1982 ◽  
Vol 156 (2) ◽  
pp. 430-442 ◽  
Author(s):  
S L Newman ◽  
J E Henson ◽  
P M Henson
Keyword(s):  
Human Monocyte ◽  
Mononuclear Phagocytes ◽  
Polymorphonuclear Neutrophils ◽  
Human Neutrophils ◽  
Dependent Manner ◽  
Blood Monocytes ◽  
Peripheral Blood Monocytes ◽  
In Vitro System ◽  
Inflammatory Macrophages

An in vitro system to investigate the ability of macrophages to recognize and ingest senescent polymorphonuclear neutrophils has been used that uses chromium-labeled neutrophils and staining for myeloperoxidase (MPO). Human monocyte-derived macrophages obtained from in vitro cultures were able to recognize "aged" but not freshly isolated 51Cr-labeled human neutrophils and ingest them. Freshly isolated monocytes did not exhibit this property. Because the aged neutrophils were greater than 95% viable, death did not appear to be a prerequisite for recognition and ingestion. Serum was not required for the aging of the neutrophils, and when serum was used, different concentrations did not appear to effect the aging process; that is, neutrophils aged in different concentrations of serum were ingested equally. Phagocytosis of senescent neutrophils by macrophages occurred in a time-dependent manner and was also dependent on the number of neutrophils added. Monocyte-derived macrophages first exhibited the ability to phagocytose senescent neutrophils on the 3rd d of culture, with the percentage of active macrophages increasing through day 7. In experiments with rabbit mononuclear phagocytes, immune complex-induced inflammatory macrophages from the lung but not resident bronchoalveolar macrophages or peripheral blood monocytes were found to be capable of recognition and ingestion of senescent rabbit neutrophils. These data suggest that the monocyte maturation process, akin to that seen during inflammation, is necessary in vitro before macrophages recognize and remove senescent neutrophils.

RANTES inhibits HIV-1 replication in human peripheral blood monocytes and alveolar macrophages

1997 ◽  
Vol 272 (5) ◽  
pp. L1025-L1029 ◽  
Author(s):  
M. J. Coffey ◽  
C. Woffendin ◽  
S. M. Phare ◽  
R. M. Strieter ◽  
D. M. Markovitz
Keyword(s):  
T Lymphocytes ◽  
Peripheral Blood ◽  
Human Peripheral Blood ◽  
Mononuclear Phagocytes ◽  
Dependent Manner ◽  
Blood Monocytes ◽  
Hiv Replication ◽  
Peripheral Blood Monocytes ◽  
Cd8 T Lymphocytes ◽  
Hiv 1

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.

scholarly journals Collagen-and collagen peptide-induced chemotaxis of human blood monocytes.

1976 ◽  
Vol 143 (6) ◽  
pp. 1299-1307 ◽  
Author(s):  
A E Postlethwaite ◽  
A H Kang
Keyword(s):  
Peripheral Blood ◽  
Degradation Products ◽  
Human Peripheral Blood ◽  
Human Neutrophils ◽  
Type I ◽  
Blood Monocytes ◽  
Peripheral Blood Monocytes ◽  
Skin Collagen ◽  
Native Collagen

The ability of collagen and collagen-derived peptides to act as chemotactic stimuli was investigated by in vitro chemotaxis assays. Native human and chick skin collagen (type I) and alpha-chains obtained from purified chick skin collagen were each chemotactic for human peripheral blood monocytes. In addition, smaller peptides obtained either by digesting native collagen with bacterial collagenase or by degrading purified alpha-chains with cyanogen bromide or pepsin were also chemotactic for monocytes. In contrast, native collagen, alpha-chains, and smaller collagen-derived peptides were not chemotactic for human neutrophils. Since collagen is degraded at sites of tissue damage and inflammation, our findings suggest the possibility that such collagen-derived degradation products might directly serve as chemotactic stimuli for human peripheral blood monocytes in vivo.

scholarly journals Human monocyte chemotaxis: migrating cells are a subpopulation with multiple chemotaxin specificities on each cell

1980 ◽  
Vol 29 (3) ◽  
pp. 953-959
Author(s):  
W Falk ◽  
E J Leonard
Keyword(s):  
Synthetic Peptide ◽  
Human Monocyte ◽  
Blood Monocytes ◽  
In Vitro System ◽  
Wide Range ◽  
Monocyte Chemotaxis ◽  
Lines Of Evidence ◽  
Number Of Cells ◽  
Migrating Cells

Only 20 to 40% of human blood monocytes were capable of responding to chemotaxins in vitro. This limit is not due to restrictions of the in vitro system, but is due to the existence of a migrating subpopulation. Over a wide range, the number of cells migrating toward a given concentration of chemotaxin was directly proportional to the number added to the chemotaxis chamber. These monocytes responded to all of the three stimuli used: human serum-derived C5a, human lymphocyte-derived chemotactic factor, and a synthetic peptide. It was possible to deactivate cells to one attractant, leaving the response to other attractants intact. This suggested that these attractants were recognized by different receptors. Several lines of evidence showed that most migrating cells had receptors for all three chemotaxins tested. Thus, if cells were assayed for migration to one attractant, no additional migration occurred when the remaining cells were assayed for migration to a different attractant. Furthermore, the same cells that had migrated toward one attractant were able to respond to other chemotaxins. We also found that a single attractant attracted as many cells as a combination of two or three attractants. Calculations from these data showed that at least 75% of the migrating monocytes have different receptors for all three attractants.

scholarly journals Crosslinking of ANCA-antigens stimulates superoxide release by human neutrophils.

1997 ◽  
Vol 8 (3) ◽  
pp. 386-394 ◽  
Author(s):  
R Kettritz ◽  
J C Jennette ◽  
R J Falk
Keyword(s):  
Polymorphonuclear Neutrophils ◽  
Tnf Alpha ◽  
Human Neutrophils ◽  
Dependent Manner ◽  
Fab Fragments ◽  
Gamma Receptor ◽  
Dose Dependent ◽  
Necrosis Factor ◽  
Neutrophil Cell

Anti-neutrophil cytoplasmic antibodies (ANCA) activate primed human polymorphonuclear neutrophils (PMN) in vitro, resulting in a respiratory burst and degranulation. In this study, the hypotheses that the initiation of this process requires engagement of the F(ab')2 portion of ANCA, and that crosslinking of ANCA target antigens is necessary to trigger superoxide (O2-) release, were explored. It is speculated that Fc gamma receptor engagement is a modulator of ANCA-mediated activation. Flow cytometry demonstrated that intact human ANCA immunoglobulin (Ig), their corresponding F(ab')2 and Fab fragments, as well as a murine monoclonal to human PR3 and its F(ab')2 fragment, bind to ANCA antigens on the surface of PMN primed with tumor necrosis factor (TNF) alpha. Intact Ig of patients with PR3-ANCA or with MPO-ANCA stimulate O2- release from TNF alpha-primed normal PMN (2.6 +/- 3.57 to 15.3 +/- 7.39 nmol O2-/2.5 x 10(6) PMN/30 min). Corresponding F(ab')2 fragments result in similar O2- production (10.2 +/- 4.34 to 36.9 nmol) in a dose-dependent manner. ANCA Fab fragments do not stimulate O2- generation until these fragments are crosslinked with F(ab')2 of goat anti-human Ig F(ab')2, or when fragments are biotinylated and crosslinked with avidin. In contrast with these human autoantibody data, a mouse monoclonal anti-human PR3 antibody (25.7 +/- 8.55 nmol O2-), but not its corresponding F(ab')2 fragment, activates TNF alpha-treated human PMN. When the Fc gamma IIa receptors were blocked, superoxide production was reduced by 33% using human PR3-ANCA Ig (P < 0.05). In conclusion, PMN activation by ANCA occurs when intact ANCA or ANCA F(ab')2 fragments crosslink target antigens on the neutrophil cell surface. ANCA F(ab') fragments result in PMN activation when crosslinked by secondary reagents.

Ultrastructural Changes in Tumor Cells During Human Peripheral Blood Monocyte-Mediated Cytotoxicity

1981 ◽  
Vol 39 ◽  
pp. 452-453
Author(s):  
K. E. Muse ◽  
D. G. Fischer ◽  
H. S. Koren
Keyword(s):  
Target Cell ◽  
Human Peripheral Blood ◽  
Mononuclear Phagocytes ◽  
Ultrastructural Changes ◽  
Target Cells ◽  
Limited Information ◽  
Blood Monocytes ◽  
Tumoricidal Activity ◽  
Activated State

Mononuclear phagocytes, a pluripotential cell line, manifest an array of basic extracellular functions. Among these physiological regulatory functions is the expression of spontaneous cytolytic potential against tumor cell targets.The limited observations on human cells, almost exclusively blood monocytes, initially reported limited or a lack of tumoricidal activity in the absence of antibody. More recently, freshly obtained monocytes have been reported to spontaneously impair the biability of tumor target cells in vitro (Harowitz et al., 1979; Montavani et al., 1979; Hammerstrom, 1979). Although the mechanism by which effector cells express cytotoxicity is poorly understood, discrete steps can be distinguished in the process of cell mediated cytotoxicity: recognition and binding of effector to target cells,a lethal-hit stage, and subsequent lysis of the target cell. Other important parameters in monocyte-mediated cytotoxicity include, activated state of the monocyte, effector cell concentrations, and target cell suseptibility. However, limited information is available with regard to the ultrastructural changes accompanying monocyte-mediated cytotoxicity.

scholarly journals Cannabidiol (CBD) Alters the Functionality of Neutrophils (PMN). Implications in the Refractory Epilepsy Treatment

2021 ◽  
Vol 14 (3) ◽  
pp. 220
Author(s):  
Claudia Taborda Gómez ◽  
Fabiana Lairion ◽  
Marisa Repetto ◽  
Miren Ettcheto ◽  
Amalia Merelli ◽  
...  
Keyword(s):  
Refractory Epilepsy ◽  
Polymorphonuclear Neutrophils ◽  
Dependent Manner ◽  
Nuclear Condensation ◽  
Concentration Dependent Manner ◽  
Superoxide Anion Production ◽  
Excretory Function ◽  
Psychoactive Effects ◽  
Stress Damage

Cannabidiol (CBD), a lipophilic cannabinoid compound without psychoactive effects, has emerged as adjuvant of anti-epileptic drugs (AEDs) in the treatment of refractory epilepsy (RE), decreasing the severity and/or frequency of seizures. CBD is considered a multitarget drug that could act throughout the canonical endocannabinoid receptors (CB1-CB2) or multiple non-canonical pathways. Despite the fact that the CBD mechanism in RE is still unknown, experiments carried out in our laboratory showed that CBD has an inhibitory role on P-glycoprotein excretory function, highly related to RE. Since CB2 is expressed mainly in the immune cells, we hypothesized that CBD treatment could alter the activity of polymorphonuclear neutrophils (PMNs) in a similar way that it does with microglia/macrophages and others circulating leukocytes. In vitro, CBD induced PMN cytoplasmatic vacuolization and proapoptotic nuclear condensation, associated with a significantly decreased viability in a concentration-dependent manner, while low CBD concentration decreased PMN viability in a time-dependent manner. At a functional level, CBD reduced the chemotaxis and oxygen consumption of PMNs related with superoxide anion production, while the singlet oxygen level was increased suggesting oxidative stress damage. These results are in line with the well-known CBD anti-inflammatory effect and support a potential immunosuppressor role on PMNs that could promote an eventual defenseless state during chronic treatment with CBD in RE.

scholarly journals In vitro formation of osteoclasts from long-term cultures of bone marrow mononuclear phagocytes.

1982 ◽  
Vol 156 (6) ◽  
pp. 1604-1614 ◽  
Author(s):  
E H Burger ◽  
J W Van der Meer ◽  
J S van de Gevel ◽  
J C Gribnau ◽  
G W Thesingh ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Electron Microscopic Examination ◽  
Osteoclast Formation ◽  
Mononuclear Phagocytes ◽  
Long Bone ◽  
Embryonic Liver ◽  
Blood Monocytes ◽  
Electron Microscopic ◽  
Embryonic Mouse

The origin of osteoclasts was studied in an in vitro model using organ cultures of periosteum-free embryonic mouse long-bone primordia, which were co-cultured with various cell populations. The bone rudiments were freed of their periosteum-perichondrium by collagenase treatment in a stage before cartilage erosion and osteoclast formation, and co-cultured for 7 d with either embryonic liver or mononuclear phagocytes from various sources. Light and electron microscopic examination of the cultures showed that mineralized matrix-resorbing osteoclasts developed only in bones co-cultured with embryonic liver or with cultured bone marrow mononuclear phagocytes but not when co-cultured with blood monocytes or resident or exudate peritoneal macrophages. Osteoclasts developed from the weakly adherent, but not from the strongly adherent cells of bone marrow cultures, whereas 1,000 rad irradiation destroyed the capacity of such cultures to form osteoclasts. In bone cultures to which no other cells were added, osteoclasts were virtually absent. Bone-resorbing activity of in vitro formed osteoclasts was demonstrated by 45Ca release studies. These studies demonstrate that osteoclasts develop from cells present in cultures of proliferating mononuclear phagocytes and that, at least in our system, monocytes and macrophages are unable to form osteoclasts. The most likely candidates for osteoclast precursor cells seem to be monoblasts and promonocytes.

scholarly journals BorreliaSpirochetes Upregulate Release and Activation of Matrix Metalloproteinase Gelatinase B (MMP-9) and Collagenase 1 (MMP-1) in Human Cells

2001 ◽  
Vol 69 (1) ◽  
pp. 456-462 ◽  
Author(s):  
Joseph A. Gebbia ◽  
James L. Coleman ◽  
Jorge L Benach
Keyword(s):  
Lyme Disease ◽  
Matrix Metalloproteinase ◽  
Human Peripheral Blood ◽  
Umbilical Vein ◽  
Active Form ◽  
Human Neutrophils ◽  
Blood Monocytes ◽  
Gelatinase B ◽  
Matrix Metalloproteinase 1

ABSTRACT Borrelia burgdorferi, the spirochetal agent of Lyme disease, stimulated human peripheral blood monocytes to release pro-matrix metalloproteinase-9 (gelatinase B; pro-MMP-9) and active matrix metalloproteinase-1 (collagenase-1; MMP-1). Human neutrophils also released pro-MMP-9 and a 130-kDa protein with gelatinolytic activity in response to live B. burgdorferi. In addition, U937 cells and human keratinocyte cells were also stimulated to release pro-MMP-9 under the same conditions. However, human umbilical vein endothelial cells (HUVECs) released pro-MMP-9 and pro-MMP-2 in a constitutive manner and were not influenced by live spirochetes. MMPs produced by human monocytes also enhanced the penetration of B. burgdorferi through extracellular matrix component barriers in vitro. Plasmin stabilized on the surface of the Lyme disease spirochete was shown to activate pro-MMP-9 to its active form. This active form was also observed in the plasma of mice infected with a relapsing fever borrelia. These results suggest that borreliae can upregulate MMPs and possibly mediate an activation cascade initiated by plasmin bound to the microbial surface. MMPs may play a role in dissemination of the Lyme disease spirochete and in the pathogenesis ofBorrelia infection.

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