摘要:

AbstractWe have analyzed peripheral blood mononuclear cell preparations from a rat model of combined injury (CI) [whole‐body irradiation (500 cGy60Co) followed by a thermal injury (20% body surface area, dorsal, scald burn)] for the expression of OX8 antigens. Ficoll‐separated mononuclear fractions were labeled with monoclonal antibodies MRC OX8, MRC OX19, W3/13 HLK, or W3/25 for flow cytometric analysis. Combined‐injury trauma resulted in decreased mononuclear cells to 6% of normal. This effect was due to the rapid decrease in radiosensitive lymphocytes from 83% to 10%. The relative numbers of monocytes increased from a normal 13% to 70% at day 4 after CI. Labeling of cells with OX8 after CI shifted to a population which was significantly larger in volume than normal lymphocytes. At the same time the mean fluorescence intensity of OX8‐positive cells was considerably reduced. With the use of a F(ab) fragment of OX8 as a probe, these results could be partially explained as unspecific binding of the whole molecule of OX8 to Fc receptors expressed by activated monocytes. But double‐labeling and cell‐sorting experiments also revealed the expression of OX8 antigens by a subset of OX8 + / OX19‐ monocytes after CI.

ISSN:0741-5400    

DOI:10.1002/jlb.42.3.181

出版商:Wiley    

年代:1987

数据来源: WILEY

摘要:

AbstractLavaged rat bronchoalveolar cells were separated into four different density fractions (I—IV) by centrifugation through a discontinuous Percoll gradient. Maximum cell size was found in the lowest density fraction (I) and minimal cell size in the highest density fraction (IV), showing an inverse correlation with cell density. These fractions contained alveolar macrophages (AM) in the proportion of 97% or more by morphologic criteria, while phagocytic AM was approximately 80% in each fraction. Although the proportion of la antigen‐positive AM was low in each fraction, it was elevated after incubation with supernatants from concanavalin A (Con A) stimulated spleen cell cultures, with greater la expression in higher density fractions. Differences in these fractions were also noted in several functions, including Fc receptor activity, chemotactic migration, tumoricidal activity, and interleukin 1 (IL‐1) production, all of which were greater in higher density fractions (III and IV). Con A‐induced T cell proliferation was, however, suppressed by these higher density fractions, whereas only an intermediate density fraction (II) enhanced T cell responses. These results indicate morphologic and functional heterogeneity among rat AM.

ISSN:0741-5400    

DOI:10.1002/jlb.42.3.188

出版商:Wiley    

年代:1987

数据来源: WILEY

摘要:

AbstractOur data establish that migration inhibition factor (MIF) and migration enhancement factor (MEF) mutually neutralize the effect of each other in a concentration‐dependent manner. The monosaccharides L‐fucose and D‐mannose were also shown to reverse MIF and additionally to stimulate alveolar macrophage (AM) migration in the absence of MIF. The specific activity of these sugars was increased 200‐fold when conjugated to bovine serum albumin (BSA). Macrophage activation is usually observed concurrently with migration inhibition when macrophages are incubated with MIF preparations. Migration inhibition occurred also when AM were incubated in the presence of known metabolic activators (MDP, PMA, and LPS). It was found that L‐fucose, D‐mannose, L‐fucosyl BSA, and D‐mannosyl BSA could reverse migration inhibition caused by MIF as well as by these metabolic activators. These observations suggest that reversal of MIF by L‐fucose is unexplained solely on the basis that L‐fucose is functioning as a competitive inhibitor; instead, they suggest that MEF and the above sugars and their conjugates stimulate AM through a receptor system different from the MIF receptor. These observations support the concept that MEF is an important macrophage modulator in CMI responses.

ISSN:0741-5400    

DOI:10.1002/jlb.42.3.197

出版商:Wiley    

年代:1987

数据来源: WILEY

摘要:

AbstractWide‐ranging differences were observed between the antitumor activities of 23 lactoba‐cilli (13 species; 23 strains) and their capacities to elevate the level of serum colony‐stimulating activity (CSA) by intraperitoneal administration in mice, and a good correlation existed between the two activities. The mechanism of enhanced production of CSA by administration ofLactobacillus caseiYIT 9018 (LC 9018), one of the bacteria that had the strongest activities, and the role of CSA in antitumor activity of LC 9018 were studied. Colony‐stimulating activity in the washing fluid from the peritoneal cavity of mice that had been administered LC 9018 intraperitoneally was elevated at 3 to 24 h after the injection, and CSA was also detected at elevated levels in the serum of the mice 6 to 12 h after injection. The cells responsible for the production of CSA after stimulation with LC 9018 seem to be the resident macrophages at the site of administration, because the resident macrophages of mice lavaged 1 h after an intraperitoneal administration of LC 9018 released CSA when they were cultured in vitro. Moreover, resident peritoneal macrophages of normal mice cultured with LC 9018 in vitro also produced CSA. Similar results were obtained with athymic nude mice, and the CSA‐inducing activity of LC 9018 was diminished in the mice pretreated with carrageenan, which is selectively toxic to mature macrophages. Bone marrow cells matured to macrophages and polymorphonuclear cells by culture with the CSA induced by LC 9018 for 7 days. These matured macrophages showed strong antitumor activity both in vivo and in vitro. These results suggest that CSA plays important roles in the antitumor activity of LC 9018: it enhances not only the multiplication of committed precursor cells for macrophages and polymorphonuclear cells, but also the functional maturation of the precursor cells for macrophages which serve as potent effectors for tumor cells.

ISSN:0741-5400    

DOI:10.1002/jlb.42.3.204

出版商:Wiley    

年代:1987

数据来源: WILEY

摘要:

AbstractWe have shown previously that the cellular proteins 47b and 71/73 could be used to construct phenotypes that distinguish among bone marrow culture‐derived (BMCD) macrophages that were either unstimulated or primed by gamma interferon or fully activated for tumor cell killing by gamma interferon in combination with lipopolysaccha‐ride (LPS). In the present study we examined in vivo‐derived correlates for each of these stages of macrophage activation and found that the same protein phenotypes held true: both p47b and p71/73 were expressed by cytolytic peritoneal macrophages, including macrophages from a tumoral effusion, whereas macrophages primed in vivo by the intraperitoneal injection of either concanavalin A or methyl vinyl ether copolymer II expressed p47b but lacked p71/73. Neither resident nor inflammatory macrophage populations expressed p47b, and acute inflammatory macrophages, like unstimulated BMCD macrophages, expressed little or no p71/73. By contrast, resident and thioglycollate‐elicited macrophages synthesized moderate levels of p71/73. When p71/73 also was expressed, there was a quantitative relationship between p47b expression and cytolytic activity in five different in vivo‐activated macrophage populations. The results suggest that, regardless of the macrophage source or stimulus, it may be possible to assess macrophage activation status by reference to protein phenotypes utilizing p47b and p71/73.

ISSN:0741-5400    

DOI:10.1002/jlb.42.3.213

出版商:Wiley    

年代:1987

数据来源: WILEY

摘要:

AbstractThe role of antigen nonspecific cytokines in T‐ and B‐lymphocyte responses is now well established, interleukin‐1 (IL‐1) has been shown to augment B‐cell maturation and proliferation. While the major source of IL‐1 is from monocytes or macrophages, other cell types have been shown to produce IL‐1‐like cytokines. Epidermal cells produce a cytokine termed “epidermal cell‐derived thymocyte‐activating factor” (ETAF) which is similar if not identical with monocyte‐derived IL‐1. In this report we show that ETAF induces polyclonal stimulation of murine B cells. We show that ETAF augments B cell proliferation and differentiation in the absence of any added antigens or mitogens. This activity can be partially inhibited by anti‐IL‐1 antibodies. ETAF appears to activate B cells directly, although its activity is increased in the presence of T cells. Thus, ETAF may be involved in local polyclonal antibody responses occurring in the skin.

ISSN:0741-5400    

DOI:10.1002/jlb.42.3.222

出版商:Wiley    

年代:1987

数据来源: WILEY

摘要:

AbstractTo elucidate changes in alveolar macrophages that accompany sepsis‐induced lung injury, this study analyzed the subfractions of alveolar macrophages (AM) recovered by lung lavage during the onset of endotoxin‐induced acute neutrophilic alveolar inflammation in the rat model. Centrifugation on continuous self‐generated density gradients of Percoll was used to fractionate AM into subpopulations between density limits 1.012 and 1.130. Two‐thirds of AM recovered from pathogen‐free control rats (group C) were in a fraction with a density range of 1.058‐1.078 [“normal” density fraction, (ND)]. Only 6% were located in a very low density (VLD) fraction 1.037‐1.048. Neutrophils accounted for less than 1% of recovered cells and usually were found in the fraction with density range of 1.079‐1.130. By contrast, if rats underwent lung lavage 15 hours after the administration of endotoxin (group E), only 38% of macrophages were recovered in the “normal” density fraction, whereas 26% of the AM recovered were in the VLD fraction. This shift in the relative sizes of the density based subpopulations coincided with the onset of acute bronchoalveolar inflammation as indicated by the recovery of neutrophils by bronchoalveolar lavage (PMN = 7 × 104in C, vs. 9.4 × 105in E, p<.001). The macrophages on the low density subfractions showed functional impairment: they were less viable in culture and migrated poorly in response to endotoxin‐activated serum compared to macrophages in the “normal” density fraction from the endotoxin‐treated animals. The rapid emergence of the low density population after endotoxin could represent an influx of new cells, but more likely indicates that injury to or previous activation of resident macrophages has caused their density to decrease. We speculate that the emergence of a population of AM in airspaces with low density and impaired function could weaken pulmonary host defense following endotoxemia.

ISSN:0741-5400    

DOI:10.1002/jlb.42.3.230

出版商:Wiley    

年代:1987

数据来源: WILEY

摘要:

AbstractThe formyl‐methionyl‐leucyl‐phenylalanine (fMet‐Leu‐Phe) dependent Ca2+uptake by human neutrophils consists of at least two components, one of which is sensitive to dihydropyridine derivatives. Inhibition by dihydropyridine derivatives showed the rank order of nisoldepine>nitrendipine>nimodepine>/Bay K 8644. The nisoldepine‐sensitive calcium uptake exhibited an ID50of 1.5 μM and maximal inhibition were observed at 5 μM. Neither calcium efflux or [3H]fMet‐Leu‐Phe binding was affected by nisoldepine up to 10 μM. The inhibition by nisoldepine was inversely proportional to the extracellular calcium concentration. Unlabeled nisoldepine and other dihydropyridine derivatives displaced the specific binding of [3H]PN 200‐110 to human neutrophils. Our data suggest a relationship between dihydropyridine binding and the inhibition of fMet‐Leu‐Phe‐dependent Ca2+uptake.

ISSN:0741-5400    

DOI:10.1002/jlb.42.3.239

出版商:Wiley    

年代:1987

数据来源: WILEY

摘要:

AbstractIn the presence of dimethyl sulfoxide (DMSO), the leukemic promyelocytic cell line HL‐60 will differentiate into mature polymorphonuclear granulocytes. In the present report, we compare chemotactic factor binding and function in HL‐60 cells with that of normal human granulocytes using the chemotactic peptide N‐formylmethionyl‐leucyl‐phenylal‐anine (FMLP) as ligand. The cellular response measured as CL was changed as a result of storage or conditioning of normal peripheral blood cells. With these cells, a conditioning procedure at room temperature resulted in a pronounced increase in the CL response. The increase of the CL response was probably a result of increased expression of cryptic receptors, since the changes of the oxidative response to FMLP was accompanied by increased binding of the peptide to the cell surface. Scatchard analysis revealed that the increased binding was due to an increased number of receptors. In differentiated HL‐60 cells, conditioning neither led to increased production of oxidative metabolites, nor to any increased binding of the peptide. The data thus indicate that many FMLP receptors could reside in a cryptic site that is not accessible to extracellular ligands, and that conditioning results in an increased exposure of these receptors, followed by an increased oxidative response to the ligand in normal cells but not in mature HL‐60 cells.

ISSN:0741-5400    

DOI:10.1002/jlb.42.3.245

出版商:Wiley    

年代:1987

数据来源: WILEY

摘要:

AbstractSubstitution of dietary fatty acids has potential for altering the inflammatory response. The purpose of the present study was to define the metabolites of arachidonic acid (AA) and eicosapentaenoic acid (EPA) secreted by bovine peripheral blood neutrophils and platelets. High performance liquid chromatography was used to characterize cyclooxygenase and lipoxygenase metabolites secreted in response to the calcium ionophore A23187. Cells were prelabelled with3H‐AA or3H‐EPA prior to challenge with the calcium ionophore. Bovine neutrophils secreted leukotriene B4(LTB4) and 5‐hydroxyeicosatet‐raenoic acid (5‐HETE) as the major metabolites of AA, as well as the corresponding leukotriene B5(LTB5) and 5‐hydroxyeicosapentaenoic acid (5‐HEPE) metabolites of EPA. Peptidoleukotrienes derived from3H‐AA or3H‐EPA were not detected under these conditions. The major tritiated metabolites secreted from bovine platelets were: thromboxane A2, measured as the stable metabolite thromboxane B2(TXB2); hydroxyhepta‐decatrienoic acid (HHT) and 12‐HETE derived from3H‐AA; and the omega‐3 analogs TXB3and 12‐HEPE, derived from3H‐EPA. Preferred substrate specificities existed amongst the AA‐ and EPA‐derived metabolites for the intermediary enzymes involved in the arachidonic acid cascade. These findings support the hypothesis that substitution of membrane‐bound AA by EPA has potential for modulation of the host inflammatory response following cellular phospholipid mobilization.

ISSN:0741-5400    

DOI:10.1002/jlb.42.3.253

出版商:Wiley    

年代:1987

数据来源: WILEY