摘要:

AbstractGuinea pig alveolar macrophages obtained by bronchoalveolar lavage were isolated by adherence for 2 h and stimulated with 1 μM ofN‐formyl‐l‐methionyl‐l‐leucyl‐l‐phenylalanine (fMLP) for different time intervals. The supernatants then were tested for their chemotactic effect on guinea pig peritoneal normodense eosinophils and for release of thromboxane B2, leukotriene B4(LTB4), and platelet activating factor (PAF). The supernatant from fMLP‐stimulated alveolar macrophages induced a significant eosinophil attraction (96.0 ± 11.9, number of migrating eosinophils [mean ± SEM],n= 17) as compared to unstimulated macrophages (4.8 ± 1.4,n= 15). This effect was not accounted for by fMLP carry‐over to the macrophages because, in contrast to human eosinophils, fMLP has no chemotactic effect on guinea pig eosinophils. Pretreatment of eosinophils with BN 52021 (100 μM), a specific PAF antagonist, and with indomethacin (10 μM), a cyclooxygenase inhibitor, failed to inhibit migration of eosinophils induced by supernatants from either stimulated or unstimulated alveolar macrophages. In contrast, inhibition of the 5‐lipoxygenase enzyme withN‐(3‐phenoxycinamyl)‐acetohydroxamic acid (1 μM) suppressed eosinophil migration by alveolar macrophage supernatants (94.1 ± 2.6% of inhibition,n= 6). Desensitization of eosinophils by and to LTB4(10 nM) inhibited migration induced by supernatants from stimulated alveolar macrophages (87.5 ± 5.4% of desensitization toward LTB4and 83.1 ± 5.4% of desensitization toward supernatants,n= 5). Under the present experimental conditions, LTB4is the only agent implicated in eosinophil migration induced by supernatants from fMLP‐stimulated alveolar macrophages.

ISSN:0741-5400    

DOI:10.1002/jlb.51.5.425

出版商:Wiley    

年代:1992

数据来源: WILEY

摘要:

AbstractWe have prepared a detergent extract from the cell wall and cell membrane ofHistoplasma capsulatumyeast cells that is recognized by T cells from mice immunized with viable organisms or with the extract. A 62‐kd antigen from this extract has been isolated and has been shown to be antigenic and to confer protective immunity in mice. In this study, we examined the in vitro proliferative response by human lymphocytes and human T‐cell clones to both the extract from the cell wall and cell membrane and the 62‐kd antigen, termed HIS‐62. Seven healthy individuals were identified whose peripheral blood mononuclear cells responded to the cell wall and cell membrane extract fromH. capsulatumyeast cells. Mononuclear cells from all seven individuals recognized histoplasmin. T‐cell clones were generated from peripheral blood mononuclear cells from a single person using the extract from cell wall and cell membrane as the antigenic preparation. Nineteen clones were propagated; all expressed the surface phenotype CD3+, CD4+, T‐cell receptor α/β+. The clones were antigen‐specific. Of 17 clones studied, none responded to extracts fromBlastomyces dermatitidisorCoccidioides immitisor to tetanus toxoid. Sixteen of 19 clones recognized HIS‐62 in vitro. Additional analysis revealed that cells from each of the seven individuals who responded to the extract mounted a proliferative response to HIS‐62. Thus, the extract from the cell wall and cell membrane and HIS‐62 are targets of the human cell‐mediated immune response to H. capsulatum. Moreover, HIS‐62 appears to be an immunodominant antigen.

ISSN:0741-5400    

DOI:10.1002/jlb.51.5.432

出版商:Wiley    

年代:1992

数据来源: WILEY

摘要:

AbstractThe cytosolic concentration of free calcium ([Ca2+]i) plays an important role in the control of many neutrophil functions. In this study, we characterize the early rapid subcellular changes in [Ca2+]ithat occur in adherent neutrophils during phagocytosis of zymosan particles, using both dual‐ and single‐excitation wavelength Fura‐2 ratio imaging. We observed a wave of elevated cytosolic calcium that began shortly after zymosan contact and propagated from the region of neutrophil contact with the zymosan throughout the cell at a rate of ≍ 17 μm/s at 31°. The wave was initiated by both opsonized and unopsonized zymosan and occurred independently of extracellular calcium. Multiple characteristics of the [Ca2+]isignal (including the absolute and regional [Ca2+]iand wave properties such as amplitude, frequency, duration, and topography) may be responsible for the differential regulation of cellular functions in the neutrophil.

ISSN:0741-5400    

DOI:10.1002/jlb.51.5.437

出版商:Wiley    

年代:1992

数据来源: WILEY

摘要:

AbstractDevelopment, differentiation, and distribution of macrophages in fetal rat lungs were investigated immunohistochemically using anti‐rat macrophage monoclonal antibodies. In the lung buds, RM‐1+macrophages were first detected on fetal day 13, and some showed reactivity for TRPM‐2. They populated in the peribronchial mesenchyme of the lung buds, proliferated in loco, and showed no peroxidase activity in any intracellular organelles. Their immunophenotypic and ultrastructural features were consistent with those of primitive/fetal macrophages. By fetal day 16, some of them expressed ED1, but ED1+cells were a minor subpopulation throughout the fetal period. On fetal day 18, ED2+macrophages developed; some also were positive for RM‐1, but the others were negative. Both the RM‐1+and ED2+macrophages were major macrophage subpopulations and expressed Ki‐M2R and/or TRPM‐3; ED2+and/or Ki‐M2R+cells are regarded as pulmonary interstitial resident macrophages. In organ culture, a similar expression of differentiation antigens by macrophages was confirmed. None of these macrophages cytochemically showed any peroxidase activity in vivo or in vitro. In the fetal stage, both RM‐1+and ED2+macrophage subpopulations showed proliferative potential, suggesting their ability to proliferate and survive in vivo.

ISSN:0741-5400    

DOI:10.1002/jlb.51.5.444

出版商:Wiley    

年代:1992

数据来源: WILEY

摘要:

AbstractPolymorphonuclear leukocytes (PMNs) recruited into the alveolar region during inflammation may injure the lung parenchyma by releasing cytotoxic oxygen radicals and proteases. Because brief exposures to crystalline silica elicit recruitment of PMNs into the alveolar region, which is strongly correlated with parameters of cytotoxicity, increased alveolar epithelial permeability, and lysosomal enzyme release, we sought to evaluate the potential role of PMNs in silica‐induced lung injury. Rats were depleted of PMNs by administration of an anti‐rat PMN antiserum prior to exposure to silica. Pulmonary inflammatory responses to silica in this group were compared to responses in normal silica‐exposed rats as well as sham‐exposed normal or PMN‐depleted rats. Bronchoalveolar lavage fluids from normal, silica‐exposed rats contained 9.7 × 106PMNs immediately after exposure for 3 days, compared to 0.01 × 106PMNs for both normal or PMN‐depleted, sham‐exposed rats. Bronchoalveolar lavage fluids from successfully PMN‐depleted, exposed rats contained significantly fewer (0.7 × 106) PMNs compared to normal silica‐exposed rats. In both groups of silica‐exposed rats, a variety of biochemical indicators of lung injury were increased significantly compared to measurements from both sham‐exposed groups, but there were no differences between PMN‐depleted and normal silica‐exposed groups. The results suggest that recruitment of PMNs into the alveolar region is not a necessary prerequisite for the observed increases in biochemical indicators of silica‐induced acute lung injury.

ISSN:0741-5400    

DOI:10.1002/jlb.51.5.455

出版商:Wiley    

年代:1992

数据来源: WILEY

摘要:

AbstractIncubation of platelet activating factor (PAF) with heparinized blood caused no induction of tissue factor activity in monocytes. However, when PAF was added in addition to weak lipopolysaccharide (LPS), it amplified the LPS effect by 80%. By using separated fresh cell populations resuspended in plasma, PAF was shown to have no enhancing effect when added to mononuclear cells incubated with platelet‐rich plasma in the presence of LPS. In contrast, when granulocytes also were included, PAF caused an almost 3‐fold increase in LPS‐induced tissue factor activity. A PAF antagonist blocked this effect and also reduced LPS‐induced tissue factor activity of monocytes in whole blood in a dose‐dependent manner. In the recombined cell incubation system, the maximal inhibition by the antagonist was observed in the presence of granulocytes. These data provide evidence for an effect of PAF on granulocytes that probably generates a product that, together with platelets, enhances LPS‐induced tissue factor activity in monocytes.

ISSN:0741-5400    

DOI:10.1002/jlb.51.5.462

出版商:Wiley    

年代:1992

数据来源: WILEY

摘要:

AbstractCarcinoembryonic antigen (CEA), a member of the immunoglobulin supergene family, is recognized by a specific 80‐kd receptor on Kupffer cells and alveolar macrophages. Peritoneal macrophages were harvested from male Sprague‐Dawley rats 72 h after intraperitoneal injection with thioglycolate broth and from unstimulated animals. The elicited peritoneal macrophages had a much greater capacity to endocytosed CEA than the cells isolated from unstimulated animals. They took up CEA in a concentration‐ and time‐dependent manner. Cellular uptake was temperature and colchicine sensitive indicating internalization of CEA. The process was saturable and could be specifically inhibited by CEA and nonspecific crossreacting antigen (NCA), a member of the CEA supergene family. Two binding proteins of ~ 35 and 80 kd were isolated from the surface of the peritoneal macrophages by affinity chromatography on a CEA‐Sepharose column. Using CEA coupled to sulfo‐succininidyl‐2‐[p‐azidosalicyl amide]‐1,3′‐dithiopropionate (SASD), a photoactivatable crosslinker, two binding proteins of 55 and 80 kd were identified on the surface of live peritoneal macrophages. The specificity of CEA endocytosis and binding proteins exhibited by the elicited peritoneal cells are similar to that previously reported for Kupffer cells and alveolar macrophages.

ISSN:0741-5400    

DOI:10.1002/jlb.51.5.466

出版商:Wiley    

年代:1992

数据来源: WILEY

摘要:

AbstractC57BL/6 mice intraperitoneally infected withMycobacterium bovisBCG (substrain Pasteur) recruited significantly higher numbers of neutrophils after an intraperitoneal inoculation of either BCG protein antigen or of endotoxin than uninfected control mice. Antigen‐induced neutrophil recruitment was mediated by T cells of both CD4+and CD8+phenotype and was also observed in the C5‐deficient DBA/2 mouse strain. The adoptive transfer of immune serum did not prime mice for enhanced antigen‐mediated recruitment of neutrophils. The endotoxin‐mediated recruitment of neutrophils was also enhanced in infected as compared to uninfected DBA/2 mice. Finally, endotoxin‐pulsed purified macrophages from infected C57BL/6 mice recruited higher numbers of neutrophils than endotoxin‐pulsed macrophages from normal mice in an adoptive transfer to peritoneal cavities of naive recipient mice. These data show that during mycobacterial infection, T cells and macrophages are primed for recruitment of neutrophils after being triggered in specific or nonspecific ways. This may represent a means to cope with secondary infections by allowing for extensive neutrophil infiltration readily upon microbial challenge.

ISSN:0741-5400    

DOI:10.1002/jlb.51.5.472

出版商:Wiley    

年代:1992

数据来源: WILEY

摘要:

Abstract(‐)Epigallocatechin gallate (EGCg) stimulated iodination of human peripheral blood monocytes, polymorphonuclear cells (PMN), and human promyelocytic leukemic HL‐60 cells, dependent on time, dose, and temperature. However, EGCg did not affect iodination of nonadherent peripheral blood mononuclear cells, red blood cells, or 11 other cultured cell lines. Although various immunoregulators such as lipopolysaccharide (LPS), opsonized zymosan, 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA) and tumor necrosis factor stimulated PMN iodination to varying degrees, their ability to stimulate monocyte iodination was much lower than that of EGCg. Washout experiments demonstrated that contact with EGCg for<60 min irreversibly stimulated PMN and monocyte iodination. EGCg also potently stimulated the production of interleukin‐1‐like factor by monocytes. The data suggest that EGCg is a strong in vitro stimulant of human phagocytes.

ISSN:0741-5400    

DOI:10.1002/jlb.51.5.478

出版商:Wiley    

年代:1992

数据来源: WILEY

摘要:

AbstractStimulation of human neutrophils with platelet activating factor (PAF) resulted in a transient elevation of free cytosolic calcium. Neutrophils exhibited a two‐component calcium response observed as a double peak when stimulated with>5 nM PAF. In contrast, leukotriene B4(LTB4), C5a, or formylmethionyl‐leucyl‐phenylalanine stimulated only a single‐peak calcium response. The double‐peak calcium response was not elicited in human monocytes or differentiated U937 cells, which demonstrated a single peak. Pretreatment of neutrophils with a 5‐lipoxygenase inhibitor or a specific LTB4‐receptor antagonist selectively blocked the second calcium peak. These results suggest that PAF‐mediated activation of human neutrophils results in the activation of the 5‐lipoxygenase and the subsequent generation of LTB4. This LTB4in turn elicits a secondary rise in calcium, which contributes to the overall response of neutrophils to PAF. These results demonstrate how LTB4participates in the cellular responses elicited by PAF in human neutrophils.

ISSN:0741-5400    

DOI:10.1002/jlb.51.5.484

出版商:Wiley    

年代:1992

数据来源: WILEY