摘要:

AbstractIn the human premonocytic line U937, 1,25‐dihydroxyvitamin D3(1,25‐(OH)2D3) induces a functional NADPH oxidase, that is responsive to both phorbol esters and opsonized zymosan. The chemotactic peptide f‐Met‐Leu‐Phe (fMLP) did not. however, induce superoxide generation by these cells. This was not due to the absence of receptors for fMLP. Although there was no significant binding of [3H]‐fMLP to undifferentiated U937 cells, preincubation with 1,25‐(OH)2D3induced expression of specific and saturable binding sites. Moreover, fMLP induced a rapid and reversible rise in cytosolic free Ca1+concentration ([Ca2+]i) in 1,25‐(OH)2D3‐treated U937 cells, but not in control or 24,25‐dihydroxyvitamin D3(24,25‐(OH)sD3)‐treated cells. This [Ca2+]iresponse was dependent on concentrations of both fMLP and 1,25‐(OH)2D3and was observed at physiologic concentrations of the hormone (25 pM). The rise in [Ca2+]iinduced by fMLP in 1,25‐(OH)2D3‐treated U937 cells was blocked by pertussis toxin and presumably mediated by inositol (1,4.5)‐trisphosphate generation. These results indicate that in U937 cells differentiated with 1,25‐(OH)2D3, inositol phosphate‐mediated [Ca2+]iresponses to fMLP are uncoupled from NADPH oxidase activation.

ISSN:0741-5400    

DOI:10.1002/jlb.45.5.381

出版商:Wiley    

年代:1989

数据来源: WILEY

摘要:

AbstractBoth purified human monocyte interleukin‐1 and recombinant interleukin‐1 (beta) primed neutrophils for increased superoxide production and chemiluminescence in response to f‐met‐leu‐phe. In addition, purified human monocyte interleukin‐1 and recombinant interleukin‐1 (beta) altered neutrophil shape. Recombinant interleukin‐1 (alpha) used at the same concentration of interleukin‐1 (beta) did not prime neutrophils for increased superoxide production after stimulation with f‐met‐leu‐phe. interleukin‐1 expressed by monocytes in response to endotoxin stimulation could act as a modulator of neutrophil function.

ISSN:0741-5400    

DOI:10.1002/jlb.45.5.389

出版商:Wiley    

年代:1989

数据来源: WILEY

摘要:

AbstractInterferon‐γ (IFN‐γ) treatment of polymorphonuclear leukocytes (PMNs) results in an activation of their functions. Studying the IFN responsiveness of PMNs and using antibodies to the IFN‐induced proteins, we have observed the ability of IFN‐α to stimulate the production of the IFN‐induced 67,000 and 56,000 dalton proteins and the ability of IFN‐γ to induce the synthesis of the 67,000, 56,000, and 42,000 dalton proteins. The induction of these proteins is dependent on de novo RNA synthesis, as its induction is inhibited if the IFNs and actinomycin D are added to the cells simultaneously. The results of this study confirm the ability of PMNs to carry out gene activation and demonstrate the ability of PMNs to respond to both IFN‐α and IFN‐γ.

ISSN:0741-5400    

DOI:10.1002/jlb.45.5.396

出版商:Wiley    

年代:1989

数据来源: WILEY

摘要:

AbstractActivation ofLeishmania enriettii‐infected mouse macrophages in vitro by treatment with macrophage activating factor (MAF)‐rich media supplemented with lipopolysaccharide (LPS) leads to rapid killing of the microorganism. When exposed to MAF + LPS in the presence of 30‐100 μM lead acetate, however, macrophages failed to destroy the parasites. This effect was not due to lead toxicity for macrophages. Decreased microbicidal activity correlated with depressed respiratory burst as determined by measurements of glucose oxidation through the hexose monophosphate shunt (HMPS). Lead had little effect on Intracellular parasite killing induced by exposure of macrophages to the electron carrier methylene blue; HMPS in such cells was similarly little affected, indicating that chemical triggering of this pathway bypassed the lead‐imposed blockade. Lead also abolished macrophage activation measured by the lysis of tumor target cells in vitro. The metal failed, however, to interfere with target‐cell lysis by macrophages activated in lead‐free medium, suggesting that lead inhibited the acquisition of the activated state rather than the functional expression of such state. Lead did not prevent the binding of radiolabelled interferon‐γ to macrophages; it did, however, slow down receptor turnover and degradation of bound interferon. Lead also inhibited the LPS‐triggered cytotoxicity in macrophages previously exposed to interferon‐γ in lead‐free medium, suggesting that depressed intracellular killing might result from an effect on both the priming (interferon or MAF‐dependent) and the triggering (LPS‐dependent) steps of activation.

ISSN:0741-5400    

DOI:10.1002/jlb.45.5.401

出版商:Wiley    

年代:1989

数据来源: WILEY

摘要:

AbstractIn order to assess the effect of Pseudorabies virus (PRV) infection on the function of swine alveolar macrophages (AM), lung lavage cells were cultured, infected with one of six strains of PRV, and various activities were measured. Activity measurement included viability, phagocytosis of yeast, phagosome‐lysosome fusion, phagocytosis of opsonized particles, and superoxide release. AM were infected with 5 × 10‐3PFU/cell, and the comparative assessment of functions was performed at 18‐20 h postinfection. Cell viability in PRV‐infected cultures ranged from 79 to 94% of the viability in noninfected cultures. Phagocytosis of yeast was significantly reduced only in the AM cultures infected with the strain S‐62. Phagosome‐lysosome fusion was depressed in cultures infected with the strains S‐62, 4892, 3816, and BUK. The phagocytosis of opsonized sheep red blood cells showed significant differences between noninfected and PRV‐infected cultures in all cases except cultures infected with the strain PRV‐C. The O2release after stimulation with opsonized zymosan was significantly reduced in all the PRV‐infected cultures. The effect of PRV infection on AM functions that are related to the bacterial activity of such cells suggests that PRV‐induced AM dysfunction might have a role in the increased susceptibility of PRV‐infected pigs to bacterial pneumonia.

ISSN:0741-5400    

DOI:10.1002/jlb.45.5.410

出版商:Wiley    

年代:1989

数据来源: WILEY

摘要:

AbstractProstaglandin E2(PGE2)‐mediated suppression of macrophage interleukin‐1α,β and tumor necrosis factor‐α synthesis was examined at the cellular and molecular levels. Treatment of lipopolysaccharide (LPS)‐stimulated adjuvant‐elicited murine macrophages with 5 × 10‐7M PGE2caused a 70% reduction in cell‐associated TNF but had no suppressive effect on cell‐associated interleukln‐1 (IL‐1) activity. Consistent with this result, Northern blot and nuclear transcription analyses demonstrated suppression of TNF mRNA but PGE2had no effect on IL‐1α and IL‐1β mRNA accumulation, as compared to LPS controls. Immunoperoxidase staining for cell‐associated TNFα, IL‐1α, and IL‐1β demonstrated that PGE2suppressed TNF, but not IL‐1α or ‐β expression, supporting the bioassay data. These results imply that PGE2‐mediated regulation of IL‐1α,β and TNFα is quite distinct. Synthesis of TNF appears to be regulated at least at the level of transcription, whereas that for IL‐1α and ‐β is regulated post‐transcriptionally.

ISSN:0741-5400    

DOI:10.1002/jlb.45.5.416

出版商:Wiley    

年代:1989

数据来源: WILEY

摘要:

AbstractThe effect of different murine monoclonal antibodies (Mab) specific for the glycoprotein complement receptor type 1 (CR1), type 2 (CR2), and type 3 (CR3) on the adhesion to and on the phagocytosis of human senescent red blood cells (S‐RBC) by monocytes or by monocyte‐derived macrophages (Mø) was investigated.Murine Mab anti‐CR3 (anti‐Leu 15 and OKM1) were found to inhibit, in the same order of magnitude, on one hand, the Fc receptors (FcR)‐dependent rosetting and phagocytosis, and, on the other hand, the S‐RBC rosetting and phagocytosis by adherent monocytes. Thus, the specific involvement of the CR3 epitopes recognized by Mab anti‐Leu 15 or by OKM1 in the interactions between S‐RBC and monocyte/macrophage could not be demonstrated.Murine Mab anti‐CR1 was found to be a significant inhibitor of binding to and of phagocytosis of S‐RBC (but not of young [Y] RBC) by monocytes or Mø, whereas Mab OKM5 carrying the same isotype as Mab anti‐CR1, but a different specificity, was devoid of any significant inhibitory effect Furthermore, Y‐RBC or S‐RBC opsonized with Mab anti‐CR1 did not form FcR‐dependent rosettes and were not internalized by monocytes; in addition, preincubation of phagocytes with Mab anti‐CR1 did not inhibit FcR‐dependent resetting and phagocytosis. These results suggest that the effect of anti‐CR1 is mediated through a specific binding to CR1 and not through an FcR blockade.As the role of specifically bound IgG on phagocytosis of human S‐RBC by macrophages has previously been demonstrated by several authors, the present study suggests that rnonocyte‐macrophage complement receptor type 1 may act in synergy with Fc receptors in the recognition of S‐RBC by macrophages. It is shown in addition that the tripeptide Arg‐Gly‐Asp, identical to the region of iC3b recognized by CR3 and by several adhesion‐promoting receptors that are structurally similar to CR3, such as fibronectin or vitronectin, is a significant inhibitor of the binding to and the phagocytosis of S‐RBC by monocytic‐macrophagic cells.

ISSN:0741-5400    

DOI:10.1002/jlb.45.5.422

出版商:Wiley    

年代:1989

数据来源: WILEY

摘要:

AbstractLangerhans cells act as antigen‐presenting cells in immune reactions in the skin. What other roles they may play in inflammation is less well defined. We have tested whether these cells can produce TNF‐alpha, an important mediator of inflammation. Resting Langerhans cells produce less than 0.1 U TNF‐alpha/ml. Langerhans cells stimulated with phorbol myristate acetate (PMA) and lipopolysaccharide (LPS) release 4‐5 U TNF‐alpha/ml. Specificity of the released TNF‐alpha in an L929 cytotoxicity assay was confirmed by using neutralizing anti‐TNF‐alpha monoclonal antibodies, and the identity of TNF‐alpha was further confirmed by Northern blot hybridization with an TNF‐alpha oligomer DNA probe. Activated Langerhans cells may contribute to inflammation in the skin by releasing TNF‐alpha, which is known to effect fibroblast growth, endothelial cell activation, and lymphocyte function.

ISSN:0741-5400    

DOI:10.1002/jlb.45.5.429

出版商:Wiley    

年代:1989

数据来源: WILEY

摘要:

AbstractBCG‐elicited mouse peritoneal macrophages were separated into three subpopulations by counterflow centrifugal elutriation. The three subpopulations were characterized on the basis of the level of a protein cross‐linking enzyme, tissue transglutaminase. Subpopulation‐3 consisted of large cells (>95% esterase positive and>90% viable) and had at least a fivefold higher transglutaminase activity (35 ± 6 nmol/hr/mg) as compared to macrophages in subpopulation‐1 (6 ± 2 nmol/hr/mg) and at least a threefold higher enzyme activity as compared to subpopulation‐2 (11 ± 2 nmol/hr/mg). Subpopulation‐3 also showed sevenfold higher phagocytosis of IgG‐coated sheep red blood cells. The three subpopulations showed no difference in their ability to killListeria monocytogenesas determined by [3H]‐thymidine release. Subpopulations‐2 and ‐3 caused 90% inhibition of murine adenocarcinoma (EMT‐6) tumor cell growth in the presence or absence of lipopolysaccharide. Subpopulation‐1 had a poor ability to inhibit EMT‐6 cell growth (29 ± 12%). However, in the presence of lipopolysaccharide, this activity increased by at least threefold (92 ± 7%). The three subpopulations showed no significant difference in their cytolytic activity against murine mastocytoma (P815) target cells in the presence or absence of lipopolysaccharide. These results suggest that tissue transglutaminase may have no significant role in bactericidal, tumoricidal, or tumoristatic function of macrophages; however, it might have some role in promoting the Fc‐receptor‐mediated phagocytic function of the macrophages.

ISSN:0741-5400    

DOI:10.1002/jlb.45.5.434

出版商:Wiley    

年代:1989

数据来源: WILEY

摘要:

AbstractIncreased production of oxidative metabolites following interaction between mononuclear phagocytes and soluble stimuli can be measured as luminol‐amplified chemiluminescence (CL). The effects of superoxide dismutase (SOD), catalase, and azide on the monocyte CL response were investigated. Azide, a myeloperoxidase (MPO) inhibitor, reduced the CL reaction by more than 80%, which indicates that the CL reaction is dependent on the granule enzyme MPO. Because SOD and catatase only partly inhibited the monocyte CL response, the authors propose that part of the monocyte CL response is of intracellular origin. This conclusion is further supported by the effects on the CL response obtained by adding extra peroxidase and the lack of correlation with techniques measuring only extracellular generated metabolites. However, it should be pointed out that the relation between extracellular and intracellular activity is stimulus dependent. Furthermore, even if quantitative differences exist between monocyte and granulocyte CL, the mechanism for the light‐generating reaction seems to be the same in both cell types.

ISSN:0741-5400    

DOI:10.1002/jlb.45.5.444

出版商:Wiley    

年代:1989

数据来源: WILEY